In the creep fatigue crack growth of GH4169 alloy,oxidation is a prominent damage source,which is mainly manifested as the oxidation damage zone in front of crack tip.In order to investigate the property of the oxidat...In the creep fatigue crack growth of GH4169 alloy,oxidation is a prominent damage source,which is mainly manifested as the oxidation damage zone in front of crack tip.In order to investigate the property of the oxidation damage zone formed in the creep fatigue crack growth,crack growth tests of directly aged GH4169 alloy were conducted at 650℃ in air under various load conditions.Interrupted tests were performed to observe the damage characteristics at crack tip.Block tests were systematically executed to quantify the dependency of oxidation damage zone size on load and holding time.The crack propagation of the GH4169 alloy has a close relationship with grain boundary oxidation at 650℃.An oxidation damage zone in front of crack tip includes intergranular microcracks and oxidised but uncracked grain boundaries.Its size has been calculated from transient crack growth rate and described as a function of maximum stress intensity factor and holding time.Based on oxidation damage zone size,a novel model has been developed to predict the creep fatigue crack growth rate of the GH4169 alloy at 650℃.展开更多
Arsenic-related oxidative stress and resultant diseases have attracted global concern,while longitudinal studies are scarce.To assess the relationship between arsenic exposure and systemic oxidative damage,we performe...Arsenic-related oxidative stress and resultant diseases have attracted global concern,while longitudinal studies are scarce.To assess the relationship between arsenic exposure and systemic oxidative damage,we performed two repeatedmeasures among 5236 observations(4067 participants)in theWuhan-Zhuhai cohort at the baseline and follow-up after 3 years.Urinary total arsenic,biomarkers of DNA oxidative damage(8-hydroxy-2-deoxyguanosine(8-OHdG)),lipid peroxidation(8-isoprostaglandin F2alpha(8-isoPGF2α)),and protein oxidative damage(protein carbonyls(PCO))were detected for all observations.Here we used linearmixed models to estimate the cross-sectional and longitudinal associations between arsenic exposure and oxidative damage.Exposure-response curves were constructed by utilizing the generalized additive mixed models with thin plate regressions.After adjusting for potential confounders,arsenic level was significantly and positively related to the levels of global oxidative damage and their annual increased rates in dose-response manners.In cross-sectional analyses,each 1%increase in arsenic levelwas associated with a 0.406%(95%confidence interval(CI):0.379%to 0.433%),0.360%(0.301%to 0.420%),and 0.079%(0.055%to 0.103%)increase in 8-isoPGF2α,8-OHdG,and PCO,respectively.More importantly,arsenic was further found to be associated with increased annual change rates of 8-isoPGF2α(β:0.147;95%CI:0.130 to 0.164),8-OHdG(0.155;0.118 to 0.192),and PCO(0.050;0.035 to 0.064)in the longitudinal analyses.Our study suggested that arsenic exposurewas not only positively related with global oxidative damage to lipid,DNA,and protein in cross-sectional analyses,but also associated with annual increased rates of these biomarkers in dose-dependent manners.展开更多
Acute lung injury(ALI)is a critical respiratory disorder with a high mortality rate and is caused by several factors.Addressing oxidative stress and infiammation is a pivotal strategy for ALI treatment.In this study,w...Acute lung injury(ALI)is a critical respiratory disorder with a high mortality rate and is caused by several factors.Addressing oxidative stress and infiammation is a pivotal strategy for ALI treatment.In this study,we introduced a novel nanotherapeutic approach involving a curcumin-loaded ceria nanoenzyme delivery system tailored to counteract the multifaceted aspects of ALI.This system leverages the individual and combined effects of the components to provide a comprehensive therapeutic solution.The dual-action capability of this nanosystem was manifested by mitigating mitochondrial oxidative stress in lung epithelial cells and inhibiting the transient receptor potential melanosome-associated protein 2(TRPM2)-NOD-like receptor thermal protein domain associated protein 3(NLRP3)signaling pathway,offering a highly effective therapeutic approach to ALI.Our findings reveal the underlying mechanisms of this innovative nanodelivery system,showcasing its potential as a versatile strategy for ALI treatment and encouraging further exploration of nanoenzyme-based therapies for ALI.展开更多
Photocatalytic disinfection is an eco-friendly strategy for countering bacterial pollution in aquatic environments.Numerous strategies have been devised to facilitate the generation of reactive oxygen species(ROS)with...Photocatalytic disinfection is an eco-friendly strategy for countering bacterial pollution in aquatic environments.Numerous strategies have been devised to facilitate the generation of reactive oxygen species(ROS)within photocatalysts,ultimately leading to the eradication of bacteria.However,the significance of the physical morphology of photocatalysts in the context of sterilization is frequently obscured,and the progress in the development of physical-chemical synergistic sterilization photocatalysts has been relatively limited.Herein,graphitic carbon nitride(g-C_(3)N_(4))is chemically protonated to expose more sharp edges.PL fluorescence and EIS results indicate that the protonation can accelerate photogenerated carrier separation and enhance ROS production.Meanwhile,the sharp edges on the protonated g-C_(3)N_(4)facilitate the physical disruption of cell walls for further promoting oxidative damage.Protonated C_(3)N_(4)demonstrated superior bactericidal performance than that of pristine g-C_(3)N_(4),effectively eliminating Escherichia coli within 40 minutes under irradiation.This work highlights the significance of incorporating physical and chemical synergies in photocatalyst design to enhance the disinfection efficiency of photocatalysis.展开更多
Deprivation of glucose and lactate provides an effective pathway to terminate the nutrients supplement for tumor growth.In this work,biomimetic nanozymes called m@BGLC are constructed for catalytic tumor inhibition th...Deprivation of glucose and lactate provides an effective pathway to terminate the nutrients supplement for tumor growth.In this work,biomimetic nanozymes called m@BGLC are constructed for catalytic tumor inhibition through nutrients deprivation and oxidative damage induction.Concretely,the catalytic enzymes of glucose oxidase(GOx),lactate oxidase(LOx)and chloroperoxidase(CPO)are precrosslinked with bovine serum albumin(BSA)to construct nanozymes,which are then biomimetic functionalized with cancer cell membrane to prepare m@BGLC.Benefiting from the biomimetic camouflage with homologous cell membrane,m@BGLC inherit homotypic binding and immune escape abilities,facilitating the tumor targeting accumulation and preferable cell internalization for improved drug delivery efficiency.Subsequently,under the cascade catalysis of nanozymes,m@BGLC consume glucose and lactate for tumor starvation therapy through nutrients deprivation,and meanwhile,the resulting hyprochloric acid(HClO)causes an oxidative damage of cells to synergistically inhibit tumor growth.In vitro and in vivo findings demonstrate a robust tumor eradication effect of m@BGLC without obvious adverse reactions via the targeted combination therapy.Such cascade catalytic nanomedicine may inspire the development of sophisticated strategies for tumor combination therapy under unfavorable tumor microenvironments.展开更多
Although it is known that the accumulation of methylglyoxal(MGO)and advanced glycosylation end products(AGEs)results in oxidative injury,the comparison between caffeic acid(CA)and chlorogenic acid(CGA)against oxidativ...Although it is known that the accumulation of methylglyoxal(MGO)and advanced glycosylation end products(AGEs)results in oxidative injury,the comparison between caffeic acid(CA)and chlorogenic acid(CGA)against oxidative damage remains unclear.Therefore,this study was conducted to compare the effects of CA and CGA using PC12 cells and Caenorhabditis elegans.The antioxidant regulatory targets for CA and CGA were primarily detected in the NRF2 pathway as predicted by network pharmacology.First,CA exerted higher effects than CGA in increasing cell viability and mitochondrial membrane potential,reducing ROS production and apoptosis,and promoting the expression of NRF2 translocation and downstream genes,which were consistent with the results of molecular docking,molecular dynamics,and covariance matrix simulations.Second,treatment with ML385(Nrf2 inhibitor)eliminated the anti-cytotoxic effect and ROS accumulation reduction effect of CA and CGA.Third,CA exhibited stronger capacities in extending lifespan,inhibiting ROS production,and increasing SKN-1 proportion than CGA in C.elegans.Multi-spectroscopy analysis also revealed a stronger inhibitory effect of CA on the formation of AGEs than that of CGA,which might be related to the alteration of the proteinα-helix.Therefore,considering the higher antioxidant effects of CA,it can be used as a promising antioxidant natural drug resource.展开更多
Metal ions trigger Fenton/Fenton-like reactions,generating highly toxic hydroxyl radicals(•OH)for chemodynamic therapy(CDT),which is crucial in inducing lethal oxidative DNA damage and subsequent cell apoptosis.Howeve...Metal ions trigger Fenton/Fenton-like reactions,generating highly toxic hydroxyl radicals(•OH)for chemodynamic therapy(CDT),which is crucial in inducing lethal oxidative DNA damage and subsequent cell apoptosis.However,tumor cells can counteract this damage through repair pathways,particularly MutT homolog 1(MTH1)protein attenuation of oxidative DNA damage.Suppression of MTH1 can enhance CDT efficacy,therefore,orderly integrating Fenton/Fenton-like agents with an MTH1 inhibitor is expected to significantly augment CDT effectiveness.Carrier-free CuTH@CD,self-assembled through the supramolecular orchestration ofγ-cyclodextrin(γ-CD)with Cu^(2+)and the MTH1 inhibitor TH588,effectively overcoming tumor resistance by greatly amplifying oxidative damage capability.Without additional carriers and mediated by multiple supramolecular regulatory effects,CuTH@CD enables high drug loading content,stability,and uniform size distribution.Upon internalization by tumor cells,CuTH@CD invalidates repair pathways through Cu^(2+)-mediated glutathione(GSH)depletion and TH588-mediated MTH1 inhibition.Meanwhile,both generated Cu^(+)ions and existing ones within the nanoassembly initiate a Fentonlike reaction,leading to the accumulation of•OH.This strategy enhances CDT efficiency with minimal side effects,improving oxidative damage potency and advancing self-delivery nanoplatforms for developing effective chemodynamic tumor therapies.展开更多
BACKGROUND:Melatonin (N-acetyl-5-methoxytripta-mine) is a free radical scavenger and a strong antioxidant,secreted by the pineal gland.In this study,we evaluated the effects of decreasing and increasing serum melatoni...BACKGROUND:Melatonin (N-acetyl-5-methoxytripta-mine) is a free radical scavenger and a strong antioxidant,secreted by the pineal gland.In this study,we evaluated the effects of decreasing and increasing serum melatonin levels on malonyldialdehyde (MDA),superoxide dismutase (SOD),and reduced glutathione (GSH) levels in pancreatic tissue from rats with experimental acute pancreatitis.METHODS:Experimental acute pancreatitis was induced in three groups of Wistar albino rats (10 animals per group) by pancreatic ductal ligation.The first group had only acute pancreatitis and served as the control.Surgical pinealectomy was added to acute pancreatitis in the second group,removing the source of endogenous melatonin (low melatonin levels group).The third group was given 0.1 ml daily intraperitoneal injections of 20 mg/ml melatonin solution for one week (high melatonin levels group).The effects of melatonin levels were evaluated by comparison of the levels of MDA,SOD,and GS in pancreatic tissue.RESULT:We found that intraperitoneal melatonin injections decreased the levels of MDA and increased the levels of SOD and GSH in pancreatic tissue.CONCLUSION:Exogenous melatonin has a preventive effect on lipid peroxidation and oxidative damage in acute pancreatitis.展开更多
Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pat...Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pathway predicted by network pharmacology.And the antioxidant effect and mechanism of hyperoside and quercetin were measured and compared in H_(2)O_(2)-induced Hep G2 cells and Caenorhabditis elegans.The findings indicated that quercetin was more effective than hyperoside in reducing oxidative damage,which was proved by improved cell viability,decreased reactive oxygen species(ROS)production,decreased cellular apoptosis,and alleviated mitochondrial damage.In addition,quercetin was more efficient than hyperoside in enhancing the expression of Nrf2-associated m RNAs,increasing the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT),and reducing the cellular malondialdehyde(MDA)content.Quercetin was superior to hyperoside in prolonging the lifespan of worms,decreasing the accumulation of lipofuscin,inhibiting ROS production,and increasing the proportion of skn-1 in the nucleus.With the Nrf2 inhibitor ML385,we verified that quercetin and hyperoside primarily protected the cells against oxidative damage via the Nrf2 signalling pathway.Furthermore,molecular docking and dynamics simulations demonstrated that the quercetin-Kelch-like ECH-associated protein 1(Keap1)complex was more stable than the hyperoside-Keap1 complex.The stable structure of the complex might hinder the binding of Nrf2 and Keap1 to release Nrf2 and facilitate its entry into the nucleus to play an antioxidant role.Overall,quercetin had a better antioxidant than hyperoside.展开更多
Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brai...Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.展开更多
Roles of Marigold extracts (ME) on arsenic trioxide (ATO)-induced oxidative damage to pancreatic β-cells need to be further elucidated. In this study, NIT-1 cells were treated with different concentrations of and/or ...Roles of Marigold extracts (ME) on arsenic trioxide (ATO)-induced oxidative damage to pancreatic β-cells need to be further elucidated. In this study, NIT-1 cells were treated with different concentrations of and/or ATO, following by the cell viability was detected by CCK8 assay. Then, intracellular reactive oxygen species (ROS) levels, lipid peroxide (MDA) contents and superoxide dismutase (SOD) activity were measured with a fluorescence probe method and colorimetric assay, respectively. The apoptosis rate and morphology was detected and observed with hoechst 33,258 staining assay. The mRNA levels and protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were measured by real-time fluorescence quantitative polymerase chain reaction and protein immunoblotting assay, respectively. Our results indicated that Co-treatment with ME and ATO exacerbated the cell viability decreasing reduced by ATO, while the addition of ME after ATO treatment effectively promote the recovery of ATO reduced survival rates. The ATO group increased apoptosis (P P β-cells by modulating the activation of the Nrf2 signaling pathway.展开更多
Objective This report aims to describe the oxidative damage profile in brain ofpresenilinl andpresenilin2 conditional double knockout mice （dKO） at both early and late age stages, and to discuss the correlation betw...Objective This report aims to describe the oxidative damage profile in brain ofpresenilinl andpresenilin2 conditional double knockout mice （dKO） at both early and late age stages, and to discuss the correlation between oxidative stress and the Alzheimer-like phenotypes of dKO mice. Methods The protein level of Aβ42 in dKO cortex and free 8-OHdG level in urine were measured by ELISA. Thiobarbituric acid method and spectrophotometric DNPH assay were used to determine the lipid peroxidation and protein oxidation in cortex, respectively. SOD and GSH-PX activities were assessed by SOD Assay Kit-WST and GSH-PX assay kit, separately. Results Significant decrease of Aβ42 was verified in dKO cortex at 6 months as compared to control mice. Although lipid peroxidation （assessed by MDA） was increased only in dKO cortex at 3 months and protein oxidation （assessed by carbonyl groups） was basically unchanged in dKO cortex, ELISA analysis revealed that free 8-OHdG, which was an indicator of DNA lesion, was significantly decreased in urine of dKO mice from 3 months to 1 2 months. Activities of SOD and GSH-PX in dKO and control cortices showed no statistical difference except a significant increase of GSH-PX activity in dKO mice at 9 months. Conclusion Oxidative damage, especially DNA lesion, was correlated with the neurodegenerative symptoms that appeared in dKO mice without the deposition of Aβ42. Triggers of oxidative damage could be the inflammatory mediators released by activated microglia and astrocytes.展开更多
Heat stress hinders the growth and productivity of sweetpotato plants,predominantly through oxidative damage to cellular membranes.Therefore,the development of efficient approaches for mitigating heat-related impairme...Heat stress hinders the growth and productivity of sweetpotato plants,predominantly through oxidative damage to cellular membranes.Therefore,the development of efficient approaches for mitigating heat-related impairments is essential for the long-term production of sweetpotatoes.Melatonin has been recognised for its capacity to assist plants in dealing with abiotic stress conditions.This research aimed to investigate how different doses of exogenous melatonin influence heat damage in sweetpotato plants.Heat stress drastically affected shoot and root fresh weight by 31.8 and 44.5%,respectively.This reduction resulted in oxidative stress characterised by increased formation of hydrogen peroxide(H_(2)O_(2))by 804.4%,superoxide ion(O_(2)^(·-))by 211.5%and malondialdehyde(MDA)by 234.2%.Heat stress also reduced chlorophyll concentration,photosystemⅡefficiency(F_v/F_m)by 15.3%and gaseous exchange.However,pre-treatment with 100μmol L^(-1)melatonin increased growth and reduced oxidative damage to sweetpotato plants under heat stress.In particular,melatonin decreased H_(2)O_(2),O_(2)^(·-)and MDA by 64.8%,42.7%and 38.2%,respectively.Melatonin also mitigated the decline in chlorophyll levels and improved stomatal traits,gaseous exchange and F_(v)/F_(m)(13%).Results suggested that the favorable outcomes of melatonin treatment can be associated with elevated antioxidant enzyme activity and an increase in non-enzymatic antioxidants and osmo-protectants.Overall,these findings indicate that exogenous melatonin can improve heat stress tolerance in sweetpotatoes.This stu dy will assist re searchers in further investigating how melatonin makes sweetpotatoes more resistant to heat stress.展开更多
Excessive accumulation of cadmium (Cd) impairs crop growth by inducing oxidative damage through the generation of reactive oxygen species (ROS). In this study, a biocompatible ferruginated carbon quantum dots (Fe-CQDs...Excessive accumulation of cadmium (Cd) impairs crop growth by inducing oxidative damage through the generation of reactive oxygen species (ROS). In this study, a biocompatible ferruginated carbon quantum dots (Fe-CQDs) nanozyme is developed to target ROS, thereby reducing oxidative damage and improving the absorption and transfer of Cd ions in wheat. Notably, Fe-CQDs exhibit multi-enzyme activities mimicking peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD), enabling effective neutralization of active species such as hydroxyl radicals (•OH), hydrogen peroxide (H_(2)O_(2)), and superoxide anions (O_(2)•^(-)). Importantly, root application of 10 mg L^(-1) Fe-CQDs alleviates Cd stress and promotes wheat growth in both hydroponic and soil cultures. Specifically, the levels of O_(2)•^(-), H_(2)O_(2), and malondialdehyde (MDA) in leaf tissues decrease, whereas the non-enzyme antioxidant, reduced glutathione (GSH), increases. Cell wall thickness in the Fe-CQDs-treated group is reduced by 42.4% compared with the Cd group. Moreover, Fe-CQDs enhance the expression of genes related to antioxidants, stress resistance, Cd detoxification, and nutrient transport. Transcriptomic and metabolomic analyses show that Fe-CQDs stimulate the production of flavonoids and regulate the activity of metal transporter genes (YSL, ABC, ZIP) to maintain ROS homeostasis. These findings highlight the potential of Fe-CQDs nanozyme platforms in mitigating oxidative damage and enhancing crop growth, offering new insights into the application of nanobiotechnology in agriculture.展开更多
Objective To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells. Methods SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate...Objective To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells. Methods SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate dehydrogenase （LDH） release and by 4＇, 6-diamidino-2-phenylindole （DAPI） staining. The cytosolic calcium concentration was tested by calcium influx assay. The glutamate-induced oxidative stress was analyzed by cytosolic glutathione assay, superoxide dismutase （SOD） assay and extracellular malondialdehyde （MDA） assay. Results Glutamate treatment caused damage in SH- SY5Y cells, including the decrease of cell viability, the increase of LDH release and the alterations of morphological structures. Furthermore, the concentration of cytoplasmic calcium in SH-SY5Y cells was not changed within 20 min following glutamate treatment, while cytosolic calcium concentration significantly increased within 24 h after glutamate treatment, which could not be inhibited by MK801, an antagonist of NMDA receptors, or by LY341495, an antagonist of metabotropic glutamate receptors. On the other hand, oxidative damage was observed in SH-SY5Y cells treated with glutamate, including decreases in glutathione content and SOD activity, and elevation of MDA level, all of which could be alleviated by an antioxidant Tanshinone IIA （Tan IIA, a major active ingredient from a Chinese plant Salvia Miltiorrhiza Bge）. Conclusion Glutamate exerts toxicity in human neuroblastoma SH-SY5Y cells possibly through oxidative damage, not through calcium homeostasis destruction mediated by NMDA receptors.展开更多
Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty ...Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.展开更多
Background:Deoxynivalenol(DON)is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals.Resveratrol(RES)effectively exerts anti-inflammatory and antioxidant effects.Howe...Background:Deoxynivalenol(DON)is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals.Resveratrol(RES)effectively exerts anti-inflammatory and antioxidant effects.However,the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear.Therefore,this study aimed to investigate the effect of RES on growth performance,gut health and the gut microbiota in DON-challenged piglets.A total of 64 weaned piglets[Duroc×(Landrace×Yorkshire),21-d-old,6.97±0.10 kg body weight(BW)]were randomly allocated to 4 treatment groups(8 replicate pens per treatment,each pen containing 2 males;n=16 per treatment)for 28 d.The piglets were fed a control diet(CON)or the CON diet supplemented with 300 mg RES/kg diet(RES group),3.8 mg DON/kg diet(DON)or both(DON+RES)in a 2×2 factorial design.Results:DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha(TNF-α)and interleukin 1 beta(IL-1β)mRNA and protein expression,and increased zonula occludens-1(ZO-1)mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet(P<0.05).Compared with unsupplemented DON-challenged piglets,infected piglets fed a diet with RES showed significantly decreased malondialdehyde(MDA)levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes(i.e.,GCLC,GCLM,HO-1,SOD1 and NQO-1)and glutamatecysteine-ligase modulatory subunit(GCLM)protein expression(P<0.05).Moreover,RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets(P<0.05).Finally,RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations,while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone(P<0.05).Conclusions:RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function,alleviating intestinal inflammation and oxidative damage,and positively modulating the gut microbiota.The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations,and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.展开更多
Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enro...Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.展开更多
Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage an...Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. Methods 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. Results Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P<0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P<0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P<0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P<0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453. Conclusion The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.展开更多
To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operato...To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operators. Methods 67 copying operators (CO) and 67 healthy volunteers (HV) were enrolled in a random control study, in which levels of lipoperoxide (LPO) in plasma and erythrocytes, and levels of vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined by spectrophotometric methods. Results Compared with the HV group, the average values of LPO in plasma and erythrocytes in the CO group were significantly increased (P<0.0001), while those of VC, VE and b-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CO group were significantly decreased (P<0.0001). Pearson product-moment correlation analysis showed that with increase of ozone level in copying sites and duration of exposure to ozone, the values of LPO in plasma and erythrocytes in the bodies of operators were gradually increased,while those of VC, VE, b-CAR, SOD, CAT and GPX were decreased in the same manner. Odds ratio (OR) of risk of biochemical parameters reflecting potential oxidative damage of the copying operators ranged from 4.440 to 13.516, and 95 % CI of OR was from 2.113 to 34.061. Reliability coefficient () of the biochemical parameters used to reflect the potential oxidative damage of the operators was 0.8156, standardized item =0.9929, P<0.0001. Conclusion Findings in the present study suggest that there exist a series of free radical chain reactions and pathological oxidative stress induced by high dose ozone in the operators, thereby causing potential oxidative and lipoperoxidative damages in their bodies.展开更多
基金supported by the National Key R&D Program of China(No.2022YFF0609300)the National Major Science and Technology Projects of China(J2019-VI-0021-0137).
文摘In the creep fatigue crack growth of GH4169 alloy,oxidation is a prominent damage source,which is mainly manifested as the oxidation damage zone in front of crack tip.In order to investigate the property of the oxidation damage zone formed in the creep fatigue crack growth,crack growth tests of directly aged GH4169 alloy were conducted at 650℃ in air under various load conditions.Interrupted tests were performed to observe the damage characteristics at crack tip.Block tests were systematically executed to quantify the dependency of oxidation damage zone size on load and holding time.The crack propagation of the GH4169 alloy has a close relationship with grain boundary oxidation at 650℃.An oxidation damage zone in front of crack tip includes intergranular microcracks and oxidised but uncracked grain boundaries.Its size has been calculated from transient crack growth rate and described as a function of maximum stress intensity factor and holding time.Based on oxidation damage zone size,a novel model has been developed to predict the creep fatigue crack growth rate of the GH4169 alloy at 650℃.
基金supported by the National Natural Science Foundation of China(Nos.82241088 and 82203996)the China Postdoctoral Science Foundation(Nos.2022T150230 and 2021M691131).
文摘Arsenic-related oxidative stress and resultant diseases have attracted global concern,while longitudinal studies are scarce.To assess the relationship between arsenic exposure and systemic oxidative damage,we performed two repeatedmeasures among 5236 observations(4067 participants)in theWuhan-Zhuhai cohort at the baseline and follow-up after 3 years.Urinary total arsenic,biomarkers of DNA oxidative damage(8-hydroxy-2-deoxyguanosine(8-OHdG)),lipid peroxidation(8-isoprostaglandin F2alpha(8-isoPGF2α)),and protein oxidative damage(protein carbonyls(PCO))were detected for all observations.Here we used linearmixed models to estimate the cross-sectional and longitudinal associations between arsenic exposure and oxidative damage.Exposure-response curves were constructed by utilizing the generalized additive mixed models with thin plate regressions.After adjusting for potential confounders,arsenic level was significantly and positively related to the levels of global oxidative damage and their annual increased rates in dose-response manners.In cross-sectional analyses,each 1%increase in arsenic levelwas associated with a 0.406%(95%confidence interval(CI):0.379%to 0.433%),0.360%(0.301%to 0.420%),and 0.079%(0.055%to 0.103%)increase in 8-isoPGF2α,8-OHdG,and PCO,respectively.More importantly,arsenic was further found to be associated with increased annual change rates of 8-isoPGF2α(β:0.147;95%CI:0.130 to 0.164),8-OHdG(0.155;0.118 to 0.192),and PCO(0.050;0.035 to 0.064)in the longitudinal analyses.Our study suggested that arsenic exposurewas not only positively related with global oxidative damage to lipid,DNA,and protein in cross-sectional analyses,but also associated with annual increased rates of these biomarkers in dose-dependent manners.
基金funded by the National Natural Science Foundation of China(Nos.82103885,81871521,82273672)Natural Science Foundation of Shanghai(Nos.21ZR1477700,20ZR1470300)+1 种基金the Shanghai Municipal Health Commission-Outstanding Youth Foundation of Public Health(No.GWV-10.2-YQ48)Sci Tech Funding by CSPFTZ Lingang Special Area Marine Biomedical Innovation Platform。
文摘Acute lung injury(ALI)is a critical respiratory disorder with a high mortality rate and is caused by several factors.Addressing oxidative stress and infiammation is a pivotal strategy for ALI treatment.In this study,we introduced a novel nanotherapeutic approach involving a curcumin-loaded ceria nanoenzyme delivery system tailored to counteract the multifaceted aspects of ALI.This system leverages the individual and combined effects of the components to provide a comprehensive therapeutic solution.The dual-action capability of this nanosystem was manifested by mitigating mitochondrial oxidative stress in lung epithelial cells and inhibiting the transient receptor potential melanosome-associated protein 2(TRPM2)-NOD-like receptor thermal protein domain associated protein 3(NLRP3)signaling pathway,offering a highly effective therapeutic approach to ALI.Our findings reveal the underlying mechanisms of this innovative nanodelivery system,showcasing its potential as a versatile strategy for ALI treatment and encouraging further exploration of nanoenzyme-based therapies for ALI.
基金supported by the National Natural Science Foundation of China(No.2021YFC3200603)the Special Research Assistant Program,Chinese Academy of Sciences.
文摘Photocatalytic disinfection is an eco-friendly strategy for countering bacterial pollution in aquatic environments.Numerous strategies have been devised to facilitate the generation of reactive oxygen species(ROS)within photocatalysts,ultimately leading to the eradication of bacteria.However,the significance of the physical morphology of photocatalysts in the context of sterilization is frequently obscured,and the progress in the development of physical-chemical synergistic sterilization photocatalysts has been relatively limited.Herein,graphitic carbon nitride(g-C_(3)N_(4))is chemically protonated to expose more sharp edges.PL fluorescence and EIS results indicate that the protonation can accelerate photogenerated carrier separation and enhance ROS production.Meanwhile,the sharp edges on the protonated g-C_(3)N_(4)facilitate the physical disruption of cell walls for further promoting oxidative damage.Protonated C_(3)N_(4)demonstrated superior bactericidal performance than that of pristine g-C_(3)N_(4),effectively eliminating Escherichia coli within 40 minutes under irradiation.This work highlights the significance of incorporating physical and chemical synergies in photocatalyst design to enhance the disinfection efficiency of photocatalysis.
基金financial support of Guangdong Basic and Applied Basic Research Foundation(No.2022B1515020095)National Natural Science Foundation of China(No.52073140)。
文摘Deprivation of glucose and lactate provides an effective pathway to terminate the nutrients supplement for tumor growth.In this work,biomimetic nanozymes called m@BGLC are constructed for catalytic tumor inhibition through nutrients deprivation and oxidative damage induction.Concretely,the catalytic enzymes of glucose oxidase(GOx),lactate oxidase(LOx)and chloroperoxidase(CPO)are precrosslinked with bovine serum albumin(BSA)to construct nanozymes,which are then biomimetic functionalized with cancer cell membrane to prepare m@BGLC.Benefiting from the biomimetic camouflage with homologous cell membrane,m@BGLC inherit homotypic binding and immune escape abilities,facilitating the tumor targeting accumulation and preferable cell internalization for improved drug delivery efficiency.Subsequently,under the cascade catalysis of nanozymes,m@BGLC consume glucose and lactate for tumor starvation therapy through nutrients deprivation,and meanwhile,the resulting hyprochloric acid(HClO)causes an oxidative damage of cells to synergistically inhibit tumor growth.In vitro and in vivo findings demonstrate a robust tumor eradication effect of m@BGLC without obvious adverse reactions via the targeted combination therapy.Such cascade catalytic nanomedicine may inspire the development of sophisticated strategies for tumor combination therapy under unfavorable tumor microenvironments.
基金supported by the Open Project of State Key Laboratory of Food Nutrition and Safety,Tianjin University of Science&Technology(SKLFNS-KF-202201)Tianjin Food Processing Control and Safety Engineering Technology Center(GCZX202303)。
文摘Although it is known that the accumulation of methylglyoxal(MGO)and advanced glycosylation end products(AGEs)results in oxidative injury,the comparison between caffeic acid(CA)and chlorogenic acid(CGA)against oxidative damage remains unclear.Therefore,this study was conducted to compare the effects of CA and CGA using PC12 cells and Caenorhabditis elegans.The antioxidant regulatory targets for CA and CGA were primarily detected in the NRF2 pathway as predicted by network pharmacology.First,CA exerted higher effects than CGA in increasing cell viability and mitochondrial membrane potential,reducing ROS production and apoptosis,and promoting the expression of NRF2 translocation and downstream genes,which were consistent with the results of molecular docking,molecular dynamics,and covariance matrix simulations.Second,treatment with ML385(Nrf2 inhibitor)eliminated the anti-cytotoxic effect and ROS accumulation reduction effect of CA and CGA.Third,CA exhibited stronger capacities in extending lifespan,inhibiting ROS production,and increasing SKN-1 proportion than CGA in C.elegans.Multi-spectroscopy analysis also revealed a stronger inhibitory effect of CA on the formation of AGEs than that of CGA,which might be related to the alteration of the proteinα-helix.Therefore,considering the higher antioxidant effects of CA,it can be used as a promising antioxidant natural drug resource.
基金funded by Tongzhou District Health Development Research Reserve Project Foundation(No.KJ2024CX024)Natural Science Foundation of Tianjin City(No.23JCQNJC01640)+1 种基金National Natural Science Foundation of China(Nos.82304393,22404122)Beijing Nova Program(No.Z211100002121127).
文摘Metal ions trigger Fenton/Fenton-like reactions,generating highly toxic hydroxyl radicals(•OH)for chemodynamic therapy(CDT),which is crucial in inducing lethal oxidative DNA damage and subsequent cell apoptosis.However,tumor cells can counteract this damage through repair pathways,particularly MutT homolog 1(MTH1)protein attenuation of oxidative DNA damage.Suppression of MTH1 can enhance CDT efficacy,therefore,orderly integrating Fenton/Fenton-like agents with an MTH1 inhibitor is expected to significantly augment CDT effectiveness.Carrier-free CuTH@CD,self-assembled through the supramolecular orchestration ofγ-cyclodextrin(γ-CD)with Cu^(2+)and the MTH1 inhibitor TH588,effectively overcoming tumor resistance by greatly amplifying oxidative damage capability.Without additional carriers and mediated by multiple supramolecular regulatory effects,CuTH@CD enables high drug loading content,stability,and uniform size distribution.Upon internalization by tumor cells,CuTH@CD invalidates repair pathways through Cu^(2+)-mediated glutathione(GSH)depletion and TH588-mediated MTH1 inhibition.Meanwhile,both generated Cu^(+)ions and existing ones within the nanoassembly initiate a Fentonlike reaction,leading to the accumulation of•OH.This strategy enhances CDT efficiency with minimal side effects,improving oxidative damage potency and advancing self-delivery nanoplatforms for developing effective chemodynamic tumor therapies.
文摘BACKGROUND:Melatonin (N-acetyl-5-methoxytripta-mine) is a free radical scavenger and a strong antioxidant,secreted by the pineal gland.In this study,we evaluated the effects of decreasing and increasing serum melatonin levels on malonyldialdehyde (MDA),superoxide dismutase (SOD),and reduced glutathione (GSH) levels in pancreatic tissue from rats with experimental acute pancreatitis.METHODS:Experimental acute pancreatitis was induced in three groups of Wistar albino rats (10 animals per group) by pancreatic ductal ligation.The first group had only acute pancreatitis and served as the control.Surgical pinealectomy was added to acute pancreatitis in the second group,removing the source of endogenous melatonin (low melatonin levels group).The third group was given 0.1 ml daily intraperitoneal injections of 20 mg/ml melatonin solution for one week (high melatonin levels group).The effects of melatonin levels were evaluated by comparison of the levels of MDA,SOD,and GS in pancreatic tissue.RESULT:We found that intraperitoneal melatonin injections decreased the levels of MDA and increased the levels of SOD and GSH in pancreatic tissue.CONCLUSION:Exogenous melatonin has a preventive effect on lipid peroxidation and oxidative damage in acute pancreatitis.
基金supported by the Open Project Program of the State Key Laboratory of Food Nutrition and Safety,Tianjin University of Science and Technology(No.SKLFNS-KF-202201)the Open Project of the Key Laboratory of Environmental Pollution Monitoring and Disease Control,Ministry of Education,Guizhou Medical University,China(No.GMU-2022-HJZ-06)。
文摘Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pathway predicted by network pharmacology.And the antioxidant effect and mechanism of hyperoside and quercetin were measured and compared in H_(2)O_(2)-induced Hep G2 cells and Caenorhabditis elegans.The findings indicated that quercetin was more effective than hyperoside in reducing oxidative damage,which was proved by improved cell viability,decreased reactive oxygen species(ROS)production,decreased cellular apoptosis,and alleviated mitochondrial damage.In addition,quercetin was more efficient than hyperoside in enhancing the expression of Nrf2-associated m RNAs,increasing the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT),and reducing the cellular malondialdehyde(MDA)content.Quercetin was superior to hyperoside in prolonging the lifespan of worms,decreasing the accumulation of lipofuscin,inhibiting ROS production,and increasing the proportion of skn-1 in the nucleus.With the Nrf2 inhibitor ML385,we verified that quercetin and hyperoside primarily protected the cells against oxidative damage via the Nrf2 signalling pathway.Furthermore,molecular docking and dynamics simulations demonstrated that the quercetin-Kelch-like ECH-associated protein 1(Keap1)complex was more stable than the hyperoside-Keap1 complex.The stable structure of the complex might hinder the binding of Nrf2 and Keap1 to release Nrf2 and facilitate its entry into the nucleus to play an antioxidant role.Overall,quercetin had a better antioxidant than hyperoside.
基金supported by the Project of Nantong Application Plan,No.BK2011055the Project of Nantong University,No.09Z032
文摘Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.
文摘Roles of Marigold extracts (ME) on arsenic trioxide (ATO)-induced oxidative damage to pancreatic β-cells need to be further elucidated. In this study, NIT-1 cells were treated with different concentrations of and/or ATO, following by the cell viability was detected by CCK8 assay. Then, intracellular reactive oxygen species (ROS) levels, lipid peroxide (MDA) contents and superoxide dismutase (SOD) activity were measured with a fluorescence probe method and colorimetric assay, respectively. The apoptosis rate and morphology was detected and observed with hoechst 33,258 staining assay. The mRNA levels and protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were measured by real-time fluorescence quantitative polymerase chain reaction and protein immunoblotting assay, respectively. Our results indicated that Co-treatment with ME and ATO exacerbated the cell viability decreasing reduced by ATO, while the addition of ME after ATO treatment effectively promote the recovery of ATO reduced survival rates. The ATO group increased apoptosis (P P β-cells by modulating the activation of the Nrf2 signaling pathway.
基金supported by the grants from Shanghai Science and Technology Commission (06DZ19003)National Natural Science Foundation of China (30870790)supported in part by 973 Project (2009CB918402)
文摘Objective This report aims to describe the oxidative damage profile in brain ofpresenilinl andpresenilin2 conditional double knockout mice （dKO） at both early and late age stages, and to discuss the correlation between oxidative stress and the Alzheimer-like phenotypes of dKO mice. Methods The protein level of Aβ42 in dKO cortex and free 8-OHdG level in urine were measured by ELISA. Thiobarbituric acid method and spectrophotometric DNPH assay were used to determine the lipid peroxidation and protein oxidation in cortex, respectively. SOD and GSH-PX activities were assessed by SOD Assay Kit-WST and GSH-PX assay kit, separately. Results Significant decrease of Aβ42 was verified in dKO cortex at 6 months as compared to control mice. Although lipid peroxidation （assessed by MDA） was increased only in dKO cortex at 3 months and protein oxidation （assessed by carbonyl groups） was basically unchanged in dKO cortex, ELISA analysis revealed that free 8-OHdG, which was an indicator of DNA lesion, was significantly decreased in urine of dKO mice from 3 months to 1 2 months. Activities of SOD and GSH-PX in dKO and control cortices showed no statistical difference except a significant increase of GSH-PX activity in dKO mice at 9 months. Conclusion Oxidative damage, especially DNA lesion, was correlated with the neurodegenerative symptoms that appeared in dKO mice without the deposition of Aβ42. Triggers of oxidative damage could be the inflammatory mediators released by activated microglia and astrocytes.
基金supported jointly by the earmarked fund for CARS-10-GW2the key research and development program of Hainan Province(Grant No.ZDYF2020226)+1 种基金Collaborative innovation center of Nanfan and high-efficiency tropical agriculture,Hainan University(Grant No.XTCX2022NYC21)funding of Hainan University[Grant No.KYQD(ZR)22123]。
文摘Heat stress hinders the growth and productivity of sweetpotato plants,predominantly through oxidative damage to cellular membranes.Therefore,the development of efficient approaches for mitigating heat-related impairments is essential for the long-term production of sweetpotatoes.Melatonin has been recognised for its capacity to assist plants in dealing with abiotic stress conditions.This research aimed to investigate how different doses of exogenous melatonin influence heat damage in sweetpotato plants.Heat stress drastically affected shoot and root fresh weight by 31.8 and 44.5%,respectively.This reduction resulted in oxidative stress characterised by increased formation of hydrogen peroxide(H_(2)O_(2))by 804.4%,superoxide ion(O_(2)^(·-))by 211.5%and malondialdehyde(MDA)by 234.2%.Heat stress also reduced chlorophyll concentration,photosystemⅡefficiency(F_v/F_m)by 15.3%and gaseous exchange.However,pre-treatment with 100μmol L^(-1)melatonin increased growth and reduced oxidative damage to sweetpotato plants under heat stress.In particular,melatonin decreased H_(2)O_(2),O_(2)^(·-)and MDA by 64.8%,42.7%and 38.2%,respectively.Melatonin also mitigated the decline in chlorophyll levels and improved stomatal traits,gaseous exchange and F_(v)/F_(m)(13%).Results suggested that the favorable outcomes of melatonin treatment can be associated with elevated antioxidant enzyme activity and an increase in non-enzymatic antioxidants and osmo-protectants.Overall,these findings indicate that exogenous melatonin can improve heat stress tolerance in sweetpotatoes.This stu dy will assist re searchers in further investigating how melatonin makes sweetpotatoes more resistant to heat stress.
基金supported by the National Natural Science Foundation of China (3237152 and 22104102)Natural Science Foundation of Sichuan Province (2025ZNSFSC0155)+1 种基金Open Project Program (SKL-KF202416) of State Key Laboratory of Crop Gene Exploration and Utilization in Southwest ChinaTwo-Way Support Programs of Sichuan Agricultural University (P202105)
文摘Excessive accumulation of cadmium (Cd) impairs crop growth by inducing oxidative damage through the generation of reactive oxygen species (ROS). In this study, a biocompatible ferruginated carbon quantum dots (Fe-CQDs) nanozyme is developed to target ROS, thereby reducing oxidative damage and improving the absorption and transfer of Cd ions in wheat. Notably, Fe-CQDs exhibit multi-enzyme activities mimicking peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD), enabling effective neutralization of active species such as hydroxyl radicals (•OH), hydrogen peroxide (H_(2)O_(2)), and superoxide anions (O_(2)•^(-)). Importantly, root application of 10 mg L^(-1) Fe-CQDs alleviates Cd stress and promotes wheat growth in both hydroponic and soil cultures. Specifically, the levels of O_(2)•^(-), H_(2)O_(2), and malondialdehyde (MDA) in leaf tissues decrease, whereas the non-enzyme antioxidant, reduced glutathione (GSH), increases. Cell wall thickness in the Fe-CQDs-treated group is reduced by 42.4% compared with the Cd group. Moreover, Fe-CQDs enhance the expression of genes related to antioxidants, stress resistance, Cd detoxification, and nutrient transport. Transcriptomic and metabolomic analyses show that Fe-CQDs stimulate the production of flavonoids and regulate the activity of metal transporter genes (YSL, ABC, ZIP) to maintain ROS homeostasis. These findings highlight the potential of Fe-CQDs nanozyme platforms in mitigating oxidative damage and enhancing crop growth, offering new insights into the application of nanobiotechnology in agriculture.
基金supported by thegrants from National Natural Science Foundation of China(No. 30870790)Shanghai Science and Technology Commis-sion (No. 06DZ19003)in part by National Basic ResearchDevelopment Program (973) of China (No. 2009CB918402)
文摘Objective To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells. Methods SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate dehydrogenase （LDH） release and by 4＇, 6-diamidino-2-phenylindole （DAPI） staining. The cytosolic calcium concentration was tested by calcium influx assay. The glutamate-induced oxidative stress was analyzed by cytosolic glutathione assay, superoxide dismutase （SOD） assay and extracellular malondialdehyde （MDA） assay. Results Glutamate treatment caused damage in SH- SY5Y cells, including the decrease of cell viability, the increase of LDH release and the alterations of morphological structures. Furthermore, the concentration of cytoplasmic calcium in SH-SY5Y cells was not changed within 20 min following glutamate treatment, while cytosolic calcium concentration significantly increased within 24 h after glutamate treatment, which could not be inhibited by MK801, an antagonist of NMDA receptors, or by LY341495, an antagonist of metabotropic glutamate receptors. On the other hand, oxidative damage was observed in SH-SY5Y cells treated with glutamate, including decreases in glutathione content and SOD activity, and elevation of MDA level, all of which could be alleviated by an antioxidant Tanshinone IIA （Tan IIA, a major active ingredient from a Chinese plant Salvia Miltiorrhiza Bge）. Conclusion Glutamate exerts toxicity in human neuroblastoma SH-SY5Y cells possibly through oxidative damage, not through calcium homeostasis destruction mediated by NMDA receptors.
文摘Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.
基金study was provided by the National Key Research and Development Program of China(2016YFD0500501)The Project of Swine Innovation Team in Guangdong Modern Agricultural Research System(2020KJ126)+4 种基金Guangzhou Science and Technology Project(201906010021)Guangdong Provincial Department of Education(2018KTSCX244)China Agriculture Research System(CARS-35)Special Fund for Scientific Innovation Strategy-construction of High Level Academy of Agriculture Science(R2016PY-QF007)Discipline team building projects of Guangdong Academy of Agricultural Science in the 14th Five-Year Period(202106TD).
文摘Background:Deoxynivalenol(DON)is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals.Resveratrol(RES)effectively exerts anti-inflammatory and antioxidant effects.However,the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear.Therefore,this study aimed to investigate the effect of RES on growth performance,gut health and the gut microbiota in DON-challenged piglets.A total of 64 weaned piglets[Duroc×(Landrace×Yorkshire),21-d-old,6.97±0.10 kg body weight(BW)]were randomly allocated to 4 treatment groups(8 replicate pens per treatment,each pen containing 2 males;n=16 per treatment)for 28 d.The piglets were fed a control diet(CON)or the CON diet supplemented with 300 mg RES/kg diet(RES group),3.8 mg DON/kg diet(DON)or both(DON+RES)in a 2×2 factorial design.Results:DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha(TNF-α)and interleukin 1 beta(IL-1β)mRNA and protein expression,and increased zonula occludens-1(ZO-1)mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet(P<0.05).Compared with unsupplemented DON-challenged piglets,infected piglets fed a diet with RES showed significantly decreased malondialdehyde(MDA)levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes(i.e.,GCLC,GCLM,HO-1,SOD1 and NQO-1)and glutamatecysteine-ligase modulatory subunit(GCLM)protein expression(P<0.05).Moreover,RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets(P<0.05).Finally,RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations,while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone(P<0.05).Conclusions:RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function,alleviating intestinal inflammation and oxidative damage,and positively modulating the gut microbiota.The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations,and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.
文摘Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.
文摘Objective To investigate whether 3,4-methylenedioxymethamphetamine (MDMA) abuse produces another neurotoxicity which may significantly inhibit the acetylcholinesterase activity and result in severe oxidative damage and liperoxidative damage to MDMA abusers. Methods 120 MDMA abusers (MA) and 120 healthy volunteers (HV) were enrolled in an independent sample control design, in which the levels of lipoperoxide (LPO) in plasma and erythrocytes as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric methods. Results Compared with the average values of biochemical parameters in the HV group, those of LPO in plasma and erythrocytes in the MA group were significantly increased (P<0.0001), while those of SOD, CAT, GPX and AChE in erythrocytes in the MA group were significantly decreased (P<0.0001). The Pearson product-moment correlation analysis between the values of AChE and biochemical parameters in 120 MDMA abusers showed that significant linear negative correlation was present between the activity of AChE and the levels of LPO in plasma and erythrocytes (P<0.0005-0.0001), while significant linear positive correlation was observed between the activity of AchE and the activities of SOD, CAT and GPX (P<0.0001). The reliability analysis for the above biochemical parameters reflecting oxidative and lipoperoxidative damages in MDMA abusers suggested that the reliability coefficient (alpha) was 0.8124, and that the standardized item alpha was 0.9453. Conclusion The findings in the present study suggest that MDMA abuse can induce another neurotoxicity that significantly inhibits acetylcholinesterase activity and aggravates a series of free radical chain reactions and oxidative stress in the bodies of MDMA abusers, thereby resulting in severe neural, oxidative and lipoperoxidative damages in MDMA abusers.
文摘To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operators. Methods 67 copying operators (CO) and 67 healthy volunteers (HV) were enrolled in a random control study, in which levels of lipoperoxide (LPO) in plasma and erythrocytes, and levels of vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined by spectrophotometric methods. Results Compared with the HV group, the average values of LPO in plasma and erythrocytes in the CO group were significantly increased (P<0.0001), while those of VC, VE and b-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CO group were significantly decreased (P<0.0001). Pearson product-moment correlation analysis showed that with increase of ozone level in copying sites and duration of exposure to ozone, the values of LPO in plasma and erythrocytes in the bodies of operators were gradually increased,while those of VC, VE, b-CAR, SOD, CAT and GPX were decreased in the same manner. Odds ratio (OR) of risk of biochemical parameters reflecting potential oxidative damage of the copying operators ranged from 4.440 to 13.516, and 95 % CI of OR was from 2.113 to 34.061. Reliability coefficient () of the biochemical parameters used to reflect the potential oxidative damage of the operators was 0.8156, standardized item =0.9929, P<0.0001. Conclusion Findings in the present study suggest that there exist a series of free radical chain reactions and pathological oxidative stress induced by high dose ozone in the operators, thereby causing potential oxidative and lipoperoxidative damages in their bodies.
