Ferroptosis,a type of programmed cell death,represents a distinct paradigm in cell biology.It is characterized by the iron-dependent accumulation of reactive oxygen species,which induce lipid peroxidation(LPO),and is ...Ferroptosis,a type of programmed cell death,represents a distinct paradigm in cell biology.It is characterized by the iron-dependent accumulation of reactive oxygen species,which induce lipid peroxidation(LPO),and is orchestrated by the interplay between iron,lipid peroxides,and glutathione.In this review,we emphasize the frequently overlooked role of iron in LPO beyond the classical iron-driven Fenton reaction in several crucial processes that regulate cellular iron homeostasis,including iron intake and export as well as ferritinophagy,and the emerging roles of endoplasmic reticulum-resident flavoprotein oxidoreductases,especially P450 oxidoreductases,in modulating LPO.We summarize how various types of fatty acids(FAs),including saturated,monounsaturated,and polyunsaturated FAs,differentially influence ferroptosis when incorporated into phospholipids.Furthermore,we highlight the therapeutic potential of targeting LPO to mitigate ferroptosis and discuss the regulatory mechanisms of endogenous lipophilic radical-trapping antioxidants that confer resistance to ferroptosis,shedding light on therapeutic avenues for ferroptosis-associated diseases.展开更多
Ferroptosis is a new regulated cell death process executed by lipid peroxidation(LPO)of polyunsaturated fatty acids.Lipid droplets(LDs),as an important organelle for lipid storage and metabolism,are probably a major s...Ferroptosis is a new regulated cell death process executed by lipid peroxidation(LPO)of polyunsaturated fatty acids.Lipid droplets(LDs),as an important organelle for lipid storage and metabolism,are probably a major site of LPO and play critical roles in the regulation of ferroptosis.However,the detailed study on LPO in LDs has not been carried out because of the lack of LD-targeting tools for the in situ monitoring of LPO.Herein,the first LD-targeting LPO fluorescence probe(LD-LPO)has been developed.LD-LPO exhibits a rapid and selective fluorescence enhancement at 518 nm,which is unaffected by highly destructive reactive oxygen species(e.g.,hydroxyl radical)and environmental factor changes(e.g.,polarity and viscosity).LD-LPO is capable of targeting LDs and visualizing LPO within LDs in situ during erastin-or(1S,3R)-RSL3(RSL3)-induced ferroptosis.Moreover,LD-LPO has also been used to image LPO in the ferroptosis-associated non-alcoholic fatty liver disease(NAFLD),and to evaluate the medicine treatment of NAFLD with saroglitazar,demonstrating its utility for monitoring LPO levels in biosystems.The favorable analytical and imaging performance of LD-LPO may allow its application in more ferroptosisassociated physiological and pathological processes.展开更多
Objective To explore the protective effects and underlying mechanisms of H_(2)S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells.Methods Cell viability was evaluated using CCK-8...Objective To explore the protective effects and underlying mechanisms of H_(2)S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells.Methods Cell viability was evaluated using CCK-8 assay. Apoptosis was measured using flow cytometry. Reagent kits were used to detect carbonyl stress markers malondialdehyde, 4-hydroxynonenal, thiobarbituric acid reactive substances, and protein carbonylation. Aldehyde-protein adduct formation and alcohol dehydrogenase, aldehyde dehydrogenase 2, aldo-keto reductase, nuclear factor E2-related factor 2(Nrf2), and cystathionine β-synthase(CBS) expression were determined using western blotting or real-time PCR. Sulforaphane(SFP) was used to activate Nrf2. RNA interference was used to inhibit CBS expression.Results GYY4137(an H_(2)S donor) pretreatment significantly reversed the uranium-induced increase in carbonyl stress markers and aldehyde-protein adducts. GYY4137 effectively restored the uraniumdecreased Nrf2 expression, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2, accompanied by a reversal of the uranium-decreased expression of CBS and aldehyde-metabolizing enzymes. The application of CBS siRNA efficiently abrogated the SFP-enhanced effects on the expression of CBS, Nrf2 activation, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2 and concomitantly reversed the SFP-enhanced effects of the uranium-induced mRNA expression of aldehyde-metabolizing enzymes.Simultaneously, CBS siRNA reversed the SFP-mediated alleviation of the uranium-induced increase in reactive aldehyde levels, apoptosis rates, and uranium-induced cell viability.Conclusion H_(2)S induces Nrf2 activation and nuclear translocation, which modulates the expression of aldehyde-metabolizing enzymes and the CBS/H_(2)S axis. Simultaneously, the Nrf2-controlled CBS/H_(2)S axis may at least partially promote Nrf2 activation and nuclear translocation. These events form a cycleregulating mode through which H_(2)S attenuates the carbonyl stress-mediated NRK-52E cytotoxicity triggered by uranium.展开更多
Background:Cardiac fibrosis following myocardial infarction(MI)drives adverse ventricular remodeling and heart failure,with cardiac fibroblasts(CFs)playing a central role.Glutathione S-transferase mu 1(GSTM1)is an imp...Background:Cardiac fibrosis following myocardial infarction(MI)drives adverse ventricular remodeling and heart failure,with cardiac fibroblasts(CFs)playing a central role.Glutathione S-transferase mu 1(GSTM1)is an important member of the glutathione S-transferase(GSTs)family,which plays an important role in maintaining cell homeostasis and detoxification.This study investigated the role and mechanism of GSTM1 in post-MI fibrosis.Methods:Multi-omics approaches(proteomics/scRNA-seq)identified GSTM1 as a dysregulated target in post-MI fibroblasts.Using a murine coronary ligation model,we assessed GSTM1 dynamics via molecular profiling,such as Western blotting,immunofluorescence,and real-time quantitative polymerase chain reaction.Adeno-associated virus serotype 9(AAV9)-mediated cardiac-specific GSTM1 overexpression was achieved through systemic delivery.In vitro studies employed transforming growth factor-β(TGF-β)-stimulated primary fibroblasts with siRNA/plasmid interventions.Mechanistic insights were derived from transcriptomics and lipid peroxidation assays.Results:The expression of GSTM1 in mouse CFs after MI was significantly down-regulated at both transcriptional and protein levels.In human dilated cardiomyopathy(DCM)patients with severe heart failure,GSTM1 expression was decreased alongside aggravated fibrosis.Overexpression of GSTM1 in post-MI mice improved cardiac function,while significantly reducing infarct size and fibrosis compared with the control group.In vitro models demonstrated that GSTM1 markedly attenuated collagen secretion and activation of fibroblasts,as well as suppressed their proliferation and migration.Further studies revealed that GSTM1 overexpression significantly inhibited the generation of intracellular and mitochondrial reactive oxygen species(ROS)under pathological conditions,suggesting that GSTM1 exerts an antioxidative stress effect in post-infarction fibroblasts.Further investigation of molecular mechanisms indicated that GSTM1 may suppress the initiation and progression of fibrosis by modulating lipid metabolism and ferroptosis-related pathways.Overexpression of GSTM1 significantly reduced lipid peroxidation and free ferrous iron levels in fibroblasts and mitochondria,markedly decreased ferroptosis-related indicators,and alleviated oxidative lipid levels[such as 12-hydroxyeicosapentaenoic acid(HEPE)and 9-,10-dihydroxy octadecenoic acid(DHOME)]under fibrotic conditions.GSTM1 enhanced the phosphorylation of signal transducer and activator of transcription 3(STAT3),thereby upregulating the downstream expression of glutathione peroxidase 4(GPX4),reducing ROS production,and mitigating fibroblast activation and phenotypic transformation by inhibiting lipid peroxidation.Conclusions:This study identifies GSTM1 as a key inhibitor of fibroblast activation and cardiac fibrosis,highlighting its ability to target ferroptosis through redox regulation.AAV-mediated GSTM1 therapy demonstrates significant therapeutic potential for improving outcomes post-MI.展开更多
BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attentio...BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.展开更多
As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities ...As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.展开更多
Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease...Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease and cancer.Lipid-based reactive oxygen species(ROS),particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis.There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis,including the synthesis of membrane phospholipids,initiation of lipid peroxidation and clearance of lipid peroxides.In this review,we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages,as well as various ferroptosis modulators targeting lipid peroxidation,including commonly used products,natural bioactive compounds and selenocompounds.Collectively,these findings suggest the vital role of lipid peroxidation in ferroptosis,and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.展开更多
Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,L...Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,Lao B,and Qiu YY.In this article,we added the correct citations of images.展开更多
Background Polystyrene nanoplastics(PS-NPs)are becoming increasingly prevalent in the environment with great advancements in plastic products,and their potential health hazard to animals has received much attention.Se...Background Polystyrene nanoplastics(PS-NPs)are becoming increasingly prevalent in the environment with great advancements in plastic products,and their potential health hazard to animals has received much attention.Several studies have reported the toxicity of PS-NPs to various tissues and cells;however,there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes,especially livestock.Herein,porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes.Results The findings showed that different concentrations of PS-NPs(0,25,50 and 100μg/m L)entering into porcine oocytes could induce mitochondrial stress,including a significant decrease in mitochondrial membrane potential(MMP),and the destruction of the balance of mitochondrial dynamic and micromorphology.Furthermore,there was a marked increase in reactive oxygen species(ROS),which led to oocyte lipid peroxidation(LPO).PS-NPs exposure induced abnormal intracellular iron overload,and subsequently increased the expression of transferrin receptor(TfRC),solute carrier family 7 member 11(SLC7a11),and acyl-CoA synthetase long-chain family member 4(ACSL4),which resulted in ferroptosis in oocytes.PS-NPs also indu ced oocyte maturation failure,cytoskeletal dysfunction and DNA damage.Cotreatment with 5μmol/L ferrostatin-1(Fer-1,an inhibitor of ferroptosis)alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation.Conclusions In conclusion,PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism,leading to the failure of oocyte maturation.展开更多
With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll ...With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll content, photosynthetic response to light intensity and temperature, chlorophyll fluorescence characteristics and membrane lipid peroxidation in their flag leaves at the late stage of development under natural conditions in Nanjing. The results were as follows:. primary photochemical efficiency of PS II ( F-v / F-m), quantum yield of linear electron transport of PS II (phi(PSII)), electron transfer rate (ETR) in these rice varieties decreased with their decrease of chlorophyll content during this period. This kind of impediment to energy conversion induced the transfer of excessive energy to the reducing side of PS I, hence the accumulation of O-2(radical anion) and peroxidation of membrane lipid, and resulting in the accumulation of malondialdehyde (MDA), that is the destroys of photosynthetic pigments and membranes and the consequent, premature senescence. This phenomenon is variable conspicuously in different rice varieties. Under natural condition in Nanjing, F-v/F-m, phi(PSII), ETR and quenching coefficient ( qP) in japonica 9516 tolerant to photooxidation decreased less and the conversion capacity of light energy was stable, premature senescence was unlikely, and consequently the seed-setting rate was higher. While F-v/F-m, phi(PSII), ETR and photochemical qP in Shanyou 63 sensitive to photooxidation decreased more and therefore premature senescence was easy to happen, thus the seed-setting rate and yield were all reduced. The tolerance to photooxidation and premature senescence in other hybrids derived from typical two line or three line crossing laid in the middle. From the rice breeding for super-high-yield, on the basis of the good plant-type of current rice, considering both hybrid vigor and the prevention premature senescence, it would be a notable strategy to use japonica maternal line or maternal. lines with some japonica genotype as the sterile lines in rice breeding.展开更多
[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to U...[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to UV-B radiation and rare earth were studied through hydroponics in laboratory. [ Result] The results showed that under irradiation of UV-B（ T1-0.15 W/m^2 and T2-0.45 W/m^2）, chlorophyll and indole-3-acetic acid（IAA） contents firstly decreased during the stress phase （1 -5 d） and then increased during the restoration phase （6 -9 d） while contents of malonadialdehyde（MDA） and abscisic acid（ABA） gradually increased during the imposition of UV-B radiation （1 -5 d） and subsequently decreased during recovery from UV-B stress （6 -9 d） . With adding of La （III） with the concentration of 20 mg · L^-1 , the decline/dse trend of chlorophyll, IAA, MDA and ABA contents was slowed down during the stress period while the rise/decline speed was accelerated during the recovery period. [ Conclusion] It suggests that the regulation of La （ III ） on membrane lipid peroxidation and endogenous hormones could increase chlorophyll and IAA contents, improve the metabolism of reactive oxygen species （ ROS）, inhibit membrane lipid peroxidation, decrease the accumulation amount of ABA and alleviate injury of UV-B radiation to soybean seedlings. Further, the protective potential of La （ III ） was better under low UV-B radiation than under high one.展开更多
AIM To study the protective effects of tea polyphenol (TP) on cerebral ischemia reperfusion injury in rats and its scavenging oxygen free radical(OFR) activities and antilipid peroxidation in vitro . METHODS Cer...AIM To study the protective effects of tea polyphenol (TP) on cerebral ischemia reperfusion injury in rats and its scavenging oxygen free radical(OFR) activities and antilipid peroxidation in vitro . METHODS Cerebral ischemia reperfusion injury was produced by bilateral ligation of the common carotid arteries with vagus nerves and reperfusion for 45 min. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. Superoxide anion (O 2) from xanthine xanthine oxidase system and hydroxyl radical (·OH) from Fe 2+ -H 2O 2 system were determined with spectrophotometry. RESULTS During Cerebral ischemia reperfusion,TP improved the activities of superoxide dismutase ( P 【0 05), GSH peroxidase( P 【0 01) and catalase( P 【0 01), while decreasing the maiondialdchyde content in the brain( P 【0 05) and brain water content ( P 【0 01). Tea polyphenol possessed significantly scavenging effects on ·OH produced by Fenton reaction and O 2 produced by xanthine xanthine oxidase system (the IC 50 were 2 2 mmol·L -1 and 1 9 mmol·L -1 respectively). Tea polyphenol could significant inhibit the lipid peroxidation of cerbral mitochondrial membrane induced by ·OH in a concentration dependent manner. CONCLUSION The results indicate that tea polyphenol could protect the injury on cerebral ischemia reperfusion in rats for OFR, these effects may be related to its scavenging effects on oxygen free radicals and antilipid peroxidant.展开更多
The effect of weak light on the peroxidation of membrane_lipid of one_year_old cherries ( Prunus pseudocerasus L. 'Laiyang') was studied by whole_tree shading. The results showed that the net photosynthetic...The effect of weak light on the peroxidation of membrane_lipid of one_year_old cherries ( Prunus pseudocerasus L. 'Laiyang') was studied by whole_tree shading. The results showed that the net photosynthetic rate of cherry leaves under weak light was remarkably lower; the activity peroxidase (POD) increased when light intensity decreased; the activity of catalase (CAT) showed an opposite trend, and it was positively correlated with light intensity; the activity of superoxide dismutase (SOD) increased under 366 μmol·m -2 ·s -1 and 533.8 μmol·m -2 ·s -1 light intensity, but decreased under 228.8 μmol·m -2 ·s -1 and 83.9 μmol·m -2 ·s -1 light intensity. A remarkable increase of malondialdehyde (MDA), a product of membrane_lipid peroxidation, was also observed in cherry leaves when treated with weak light, indicating more serious peroxidation in the membrane.展开更多
Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light ...Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light stress conditions. Results showed that D1 protein contents of PSⅡ in photosynthetic apparatus dropped, the generation of antheraxanthin (A) and zeaxanthin (Z) of xanthophyll cycle were inhibited partly, PSⅡ photochemical efficiency (F v/F m)and non-photochemical quenching (q N) were also decreased obviously. In addition, endogenous active oxygen scavenger—superoxide dismutase (SOD) reduced, superoxide anion radical (O -· 2) and malondialdehyde (MDA) accumulated, as a result, photooxidation of leaves occurred under chilling temperature and strong light stress conditions. Obvious differences in the changes of the above mentioned physiological parameters between indica and japonica rice were observed. Experiments in leaves treated with inhibitors under chilling temperature and strong light conditions showed that indica rice was more sensitive to chilling temperature with strong light and subjected to photooxidation more than japonica rice. Notable positive correlation between D1 protein contents and F v/F m or (A+Z)/(A+Z+V), and a marked negative correlation between F v/F m and MDA contents were obtained by regression analysis in indica and japonica rice during chilling temperature and strong light conditions. According to the facts mentioned above, it was inferred that PSⅡ photochemical efficiency(F v/F m) was the key index to forecast for the prediction of photooxidation under stress circumstances and the physiological basis were the synthetic capacity of D1 protein and the protection of xanthophyll cycle.展开更多
Using various high-yield rices (Oryza sativa L.) such as japonica cultivar 9516, two parental line hybrid rice between subspecies with more japonica element Peiai 64/E32, Liangyoupeijiu (Peiai 64/9311), and indica hyb...Using various high-yield rices (Oryza sativa L.) such as japonica cultivar 9516, two parental line hybrid rice between subspecies with more japonica element Peiai 64/E32, Liangyoupeijiu (Peiai 64/9311), and indica hybrid rices X07S/Zihui 100, Gangyou 881, Shanyou 63 as the materials, the characteristics of chlorophyll fluorescence and membrane-lipid peroxidation of detached leaves at booting stage under photooxidation conditions were studied. In comparison with indica hybrid rice, after the photooxidation treatment, the primary photochemical efficiency of PS II (F-v/F-m), quantum yield of linear electron transport of PS II (Phi(PSII)) and photochemical quenching coefficient (qP) in japonica cultivar and hybrid rice with japonica decreased less. This indicated that high-yield rice with japonica was able to maintain higher capability of light energy conversion, resulting in the alleviation of photoinhibition. Meanwhile, the higher activities of protective enzymes such as superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) led to the less accumulation of endogenous active oxygen (O-(2)(radical anion), H2O2) and less content of the malondialdehyde (MDA) and the less decline of chlorophyll and protein contents, indicating a stronger tolerance to photooxidation. The changes in contents of chlorophyll and protein among various nee cultivars during photooxidation treatment were consistent with the decline of chlorophyll content from heading stage to maturation stage under natural conditions. Statistical analysis showed that there was a significant correlation between the indexes of tolerance to photooxidation and the rate of seed setting, implying that the cultivar tolerated to photooxidation had higher resistance to early aging of leaf. These results suggested that from a view of superhigh-yield breeding, considering both the utilization of heterosis and the resistance to early aging of leaf, introduction of japonica element tolerating to photooxidation into the rice sterile line (maternal plant) is a breeding strategy worthy to pay great attention to.展开更多
[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside （SNP） was selected as an exogenous nitr...[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside （SNP） was selected as an exogenous nitric oxide（NO）donor.[Method] There are 3 groups including CK,UV treatment group （B）,B＋SNP treatment group,0,1,2,3,4 d sampling after treatment respectively,and physiological and biochemical indexes of MDA content and CAT,POD,SOD and so on were determined,repeated 3 times,and statistical analyzed.[Result] The results showed that,after the enhanced UV-B radiation,activity of the catalase （CAT）,superoxide dismutase （SOD） and of the guaiacol peroxidase （POD） all reduced apparently,and the concentration of malondialdehyde （MDA） increased obviously,leading to oxidative damage in wheat seedlings.Impose different concentrations of SNP after UV-B radiation,may mitigate oxidative damage of wheat seedling from different degrees,which was in agreement with the effect of making the concentration of MDA decrease and the activity of the CAT,SOD and POD all increased.The mitigation role of 0.01 mol/L SNP was more obvious for roots＇ oxidative damage,while 0.1 mmol/L SNP is more effective for oxidative damage of leaves.[Conclusion] Exogenous NO donor SNP had obvious relieve effects on oxidative damage of wheat seedlings caused by UV-B radiation,which can enhance adaptive capacity of plants to adversity stress.展开更多
AIM:To study relationship of injury induced by nitric oxide, oxidation, peroxidation,lipoperoxidation with chronic cholecystitis.METHODS:The values of plasma nitric oxide (P-NO), plasma vitamin C (P-VC), plasma vitami...AIM:To study relationship of injury induced by nitric oxide, oxidation, peroxidation,lipoperoxidation with chronic cholecystitis.METHODS:The values of plasma nitric oxide (P-NO), plasma vitamin C (P-VC), plasma vitamin E (P-VE), plasma beta-carotene (P-beta-CAR), plasma lipoperoxides (P-LPO), erythrocyte superoxide dismutase (E-SOD), erythrocyte catalase (E-CAT), erythrocyte glutathione peroxidase (E-GSH-Px) activities and erythrocyte lipoperoxides (E-LPO) level in 77 patients with chronic cholecystitis and 80 healthy control subjects were determined, differences of the above average values between the patient group and the control group and differences of the average values between preoperative and postoperative patients were analyzed and compared, linear regression and correlation of the disease course with the above determination values as well as the stepwise regression and correlation of the course with the values were analyzed.RESULTS:Compared with the control group, the average values of P-NO, P-LPO, E-LPO were significantly increased (P【0.01), and of P-VC, P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px decreased (P 【0.01) in the patient group. The analysis of the linear regression and correlation showed that with prolonging of the course, the values of P-NO, P-LPO and E-LPO in the patients were gradually ascended and the values of P-VC,P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px descended (P【0.01). The analysis of the stepwise regression and correlation indicated that the correlation of the course with P-NO, P-VE and P-beta-CAR values was the closest. Compared with the preoperative patients, the average values of P-NO, P-LPO and E-LPO were significantly decreased (P 【0.01) and the average values of P-VC, E-SOD, E-CAT and E-GSH-Px in postoperative patients increased (P 【0.01) in postoperative patients. But there was no significant difference in the average values of P-VE, P-beta-CAR preoperative and postoperative patients.CONCLUSION:Chronic cholecystitis could induce the increase of nitric oxide, oxidation, peroxidation and lipoperoxidation.展开更多
[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein co...[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein concentration assay, enzyme activity assay and antioxidant activity determination by DPPH method, peroxide activity inhibition of in vitro tissues from mice by homogenate MDA colorimetry method and lipid peroxidation assay of in vitro tissues. [ Result ] IC50 of the crude enzyme liquid extracted from pea on DPPH was 55.16 mg/L, while the scavenging rate of the crude enzyme liquid was lower than that of ascorbic acid, tea polyphenol and citric acid with the same concentration. The synergistic effect was found in ascorbic acid and crude enzyme liquid, but the synergism of ascorbic acid was better than that of citric acid. IC50 of SOD enzyme liquid extracted from pea on DPPH was 11.1 mg/L, which was better than that of tea polyphenol and closely similar to that of ascorbic acid. SOD enzyme liquid extracted from pea had an inhibitory effect on MDA production from in vitro tissues such as liver, kidney and heart, especially for a significantly inhibitory effect on MDA from liver in vitro. When the concentration was 0.25 mg/ml, the inhibition rate reached 78.3%, and then the inhibition rate increased little with the concentration incresas, while its effect on heart and kidney were inferior. [ Conclusion] SOD crude enzyme liquid and SOD enzyme liquid extracted from pea all have certain DPPH scavenging capacity, while SOD enzyme liquid extracted from pea has an inhibitory effect on lipid peroxidation.展开更多
The main purpose of this study was to investigate the protective actions of captopril and cicaprost on changes of membrane fluidity of cultured neonatal rat myocardial cells exposed to anoxia and sugar deprivation.Lip...The main purpose of this study was to investigate the protective actions of captopril and cicaprost on changes of membrane fluidity of cultured neonatal rat myocardial cells exposed to anoxia and sugar deprivation.Lipid peroxidation level estimated by determining the thiobarbituric acid reactive substance(TBARS)content and lactate dehydrogenase(LDH)released in culture medium was also observed in order to examine other membrane-related changes due to anoxia.Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropy(r_s)by fluorescence spectroscopy.The r_s value,TBARS level and LDH release were significantly increased after 3 h anoxia.Captopril(180 μmol/L),cicaprost(30 nmol/L)and indomethacin(1μmol/L)did not alter r_s, TBARS level and LDH activity of normal cultured neonatal rat myocardial cells.However,both captopril and cicaprost significantly prevented the increases of r_s,TBARS content and LDH release in those cells exposed to anoxia and sugar deprivation.lndomethacin abolished the actions of captopril on TBARS production and LDH release,but maintained its membrane fluidity protection.These results indicate that captopril and cicaprost protect membrane fluidity and lipid peroxidation changes in anoxia- injured myocardial cells.The action mechanism of captopril may be due,in part,to stimulation of prostacyclin synthesis and/or release.展开更多
The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by ...The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe 2+ were tested by differential spectrum. Superoxide anion (O 2)from xanthine xanthine oxidase (Xan XO) system and hydroxyl radical (·OH) from FeSO 4 H 2O 2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan XO and FeSO 4 H 2O 2 system. The IC 50 of Bre were 93 01 μmol·L -1 for Xan XO system and 62 18 μmol·L -1 for FeSO 4 H 2O 2 system. Bre also scavenged O 2 and ·OH produced by Xan XO and FeSO 4 H 2O 2 systems. The IC 50 of Bre were 32 63 μmol·L -1 for O - 2 and 20 22 μmol·L -1 for ·OH. Furthermore, the chelating Fe 2+ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe 2+ and scavenging O 2 as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.展开更多
基金supported by grants from the National Natural Science Foundation of China(22076104)the“Taishan Scholars”Program for Young Expert of Shandong Province(tsqn202103105).
文摘Ferroptosis,a type of programmed cell death,represents a distinct paradigm in cell biology.It is characterized by the iron-dependent accumulation of reactive oxygen species,which induce lipid peroxidation(LPO),and is orchestrated by the interplay between iron,lipid peroxides,and glutathione.In this review,we emphasize the frequently overlooked role of iron in LPO beyond the classical iron-driven Fenton reaction in several crucial processes that regulate cellular iron homeostasis,including iron intake and export as well as ferritinophagy,and the emerging roles of endoplasmic reticulum-resident flavoprotein oxidoreductases,especially P450 oxidoreductases,in modulating LPO.We summarize how various types of fatty acids(FAs),including saturated,monounsaturated,and polyunsaturated FAs,differentially influence ferroptosis when incorporated into phospholipids.Furthermore,we highlight the therapeutic potential of targeting LPO to mitigate ferroptosis and discuss the regulatory mechanisms of endogenous lipophilic radical-trapping antioxidants that confer resistance to ferroptosis,shedding light on therapeutic avenues for ferroptosis-associated diseases.
基金the financial support from the National Natural Science Foundation of China(Nos.82060626,22004137,22164022,22174147,22074151,22374153,22174148)Excellent Youth scientific and technological talents of Guizhou Province(No.Qiankehe platform talents[2021]5638)+3 种基金Talents of Guizhou Science and Technology Cooperation Platform(No.[2020]4104)Science and Technology Innovation Team of Higher Education of Guizhou Provincial Education Department(No.Qianjiaoji[2023]073)Future Science and Technology Elite Talent Cultivation Project of Zunyi Medical University(No.ZYSE-2021-01)Zunyi Science and Technology Plan Project(No.Zunshi Keren Platform[2023]2)。
文摘Ferroptosis is a new regulated cell death process executed by lipid peroxidation(LPO)of polyunsaturated fatty acids.Lipid droplets(LDs),as an important organelle for lipid storage and metabolism,are probably a major site of LPO and play critical roles in the regulation of ferroptosis.However,the detailed study on LPO in LDs has not been carried out because of the lack of LD-targeting tools for the in situ monitoring of LPO.Herein,the first LD-targeting LPO fluorescence probe(LD-LPO)has been developed.LD-LPO exhibits a rapid and selective fluorescence enhancement at 518 nm,which is unaffected by highly destructive reactive oxygen species(e.g.,hydroxyl radical)and environmental factor changes(e.g.,polarity and viscosity).LD-LPO is capable of targeting LDs and visualizing LPO within LDs in situ during erastin-or(1S,3R)-RSL3(RSL3)-induced ferroptosis.Moreover,LD-LPO has also been used to image LPO in the ferroptosis-associated non-alcoholic fatty liver disease(NAFLD),and to evaluate the medicine treatment of NAFLD with saroglitazar,demonstrating its utility for monitoring LPO levels in biosystems.The favorable analytical and imaging performance of LD-LPO may allow its application in more ferroptosisassociated physiological and pathological processes.
基金supported by the National Natural Science Foundation of China(No.82160627)the Natural Science Foundation of the Guangxi Autonomous Region(No.2020GXNFSAA297262)。
文摘Objective To explore the protective effects and underlying mechanisms of H_(2)S against lipid peroxidation-mediated carbonyl stress in the uranium-treated NRK-52E cells.Methods Cell viability was evaluated using CCK-8 assay. Apoptosis was measured using flow cytometry. Reagent kits were used to detect carbonyl stress markers malondialdehyde, 4-hydroxynonenal, thiobarbituric acid reactive substances, and protein carbonylation. Aldehyde-protein adduct formation and alcohol dehydrogenase, aldehyde dehydrogenase 2, aldo-keto reductase, nuclear factor E2-related factor 2(Nrf2), and cystathionine β-synthase(CBS) expression were determined using western blotting or real-time PCR. Sulforaphane(SFP) was used to activate Nrf2. RNA interference was used to inhibit CBS expression.Results GYY4137(an H_(2)S donor) pretreatment significantly reversed the uranium-induced increase in carbonyl stress markers and aldehyde-protein adducts. GYY4137 effectively restored the uraniumdecreased Nrf2 expression, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2, accompanied by a reversal of the uranium-decreased expression of CBS and aldehyde-metabolizing enzymes. The application of CBS siRNA efficiently abrogated the SFP-enhanced effects on the expression of CBS, Nrf2 activation, nuclear translocation, and ratio of nuclear to cytoplasmic Nrf2 and concomitantly reversed the SFP-enhanced effects of the uranium-induced mRNA expression of aldehyde-metabolizing enzymes.Simultaneously, CBS siRNA reversed the SFP-mediated alleviation of the uranium-induced increase in reactive aldehyde levels, apoptosis rates, and uranium-induced cell viability.Conclusion H_(2)S induces Nrf2 activation and nuclear translocation, which modulates the expression of aldehyde-metabolizing enzymes and the CBS/H_(2)S axis. Simultaneously, the Nrf2-controlled CBS/H_(2)S axis may at least partially promote Nrf2 activation and nuclear translocation. These events form a cycleregulating mode through which H_(2)S attenuates the carbonyl stress-mediated NRK-52E cytotoxicity triggered by uranium.
基金supported by the National Natural Science Foundation of China(82270386,82070252,and 8207025)the Zhejiang Provincial Medical and Health Science and Technology Plan(2023RC020)the Zhejiang Provincial Natural Science Foundation(LR21H020001).
文摘Background:Cardiac fibrosis following myocardial infarction(MI)drives adverse ventricular remodeling and heart failure,with cardiac fibroblasts(CFs)playing a central role.Glutathione S-transferase mu 1(GSTM1)is an important member of the glutathione S-transferase(GSTs)family,which plays an important role in maintaining cell homeostasis and detoxification.This study investigated the role and mechanism of GSTM1 in post-MI fibrosis.Methods:Multi-omics approaches(proteomics/scRNA-seq)identified GSTM1 as a dysregulated target in post-MI fibroblasts.Using a murine coronary ligation model,we assessed GSTM1 dynamics via molecular profiling,such as Western blotting,immunofluorescence,and real-time quantitative polymerase chain reaction.Adeno-associated virus serotype 9(AAV9)-mediated cardiac-specific GSTM1 overexpression was achieved through systemic delivery.In vitro studies employed transforming growth factor-β(TGF-β)-stimulated primary fibroblasts with siRNA/plasmid interventions.Mechanistic insights were derived from transcriptomics and lipid peroxidation assays.Results:The expression of GSTM1 in mouse CFs after MI was significantly down-regulated at both transcriptional and protein levels.In human dilated cardiomyopathy(DCM)patients with severe heart failure,GSTM1 expression was decreased alongside aggravated fibrosis.Overexpression of GSTM1 in post-MI mice improved cardiac function,while significantly reducing infarct size and fibrosis compared with the control group.In vitro models demonstrated that GSTM1 markedly attenuated collagen secretion and activation of fibroblasts,as well as suppressed their proliferation and migration.Further studies revealed that GSTM1 overexpression significantly inhibited the generation of intracellular and mitochondrial reactive oxygen species(ROS)under pathological conditions,suggesting that GSTM1 exerts an antioxidative stress effect in post-infarction fibroblasts.Further investigation of molecular mechanisms indicated that GSTM1 may suppress the initiation and progression of fibrosis by modulating lipid metabolism and ferroptosis-related pathways.Overexpression of GSTM1 significantly reduced lipid peroxidation and free ferrous iron levels in fibroblasts and mitochondria,markedly decreased ferroptosis-related indicators,and alleviated oxidative lipid levels[such as 12-hydroxyeicosapentaenoic acid(HEPE)and 9-,10-dihydroxy octadecenoic acid(DHOME)]under fibrotic conditions.GSTM1 enhanced the phosphorylation of signal transducer and activator of transcription 3(STAT3),thereby upregulating the downstream expression of glutathione peroxidase 4(GPX4),reducing ROS production,and mitigating fibroblast activation and phenotypic transformation by inhibiting lipid peroxidation.Conclusions:This study identifies GSTM1 as a key inhibitor of fibroblast activation and cardiac fibrosis,highlighting its ability to target ferroptosis through redox regulation.AAV-mediated GSTM1 therapy demonstrates significant therapeutic potential for improving outcomes post-MI.
文摘BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.
文摘As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.
基金supported by Jiangxi Provincial Natural Science Foundation(20224BAB216091,20224ACB205014)Jiangxi Provincial Department of Education Science and Technology Plan Project(GJJ2200420).
文摘Ferroptosis is a novel form of cell death driven by iron-dependent lipid peroxidation and it is implicated in various diseases,such as liver disease,acute kidney injury,cardiovascular disease,neurodegenerative disease and cancer.Lipid-based reactive oxygen species(ROS),particularly lipid hydroperoxides in the cellular membrane can lead to membrane disruption and cell death mediated by ferroptosis.There are three necessary stages involving in the process of lipid peroxidation regulation in ferroptosis,including the synthesis of membrane phospholipids,initiation of lipid peroxidation and clearance of lipid peroxides.In this review,we summarized the molecular modulation mechanisms of lipid peroxidation in ferroptosis from the above three stages,as well as various ferroptosis modulators targeting lipid peroxidation,including commonly used products,natural bioactive compounds and selenocompounds.Collectively,these findings suggest the vital role of lipid peroxidation in ferroptosis,and targeting lipid peroxidation in ferroptosis is potential to treat ferroptosis-associated diseases.
文摘Correction to“Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer”in World J Gastrointest Oncol 2024;16:2335-2349,published by Shu YJ,Lao B,and Qiu YY.In this article,we added the correct citations of images.
基金supported by the National Natural Science Foundation of China(31972759 and 31572589)the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)。
文摘Background Polystyrene nanoplastics(PS-NPs)are becoming increasingly prevalent in the environment with great advancements in plastic products,and their potential health hazard to animals has received much attention.Several studies have reported the toxicity of PS-NPs to various tissues and cells;however,there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes,especially livestock.Herein,porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes.Results The findings showed that different concentrations of PS-NPs(0,25,50 and 100μg/m L)entering into porcine oocytes could induce mitochondrial stress,including a significant decrease in mitochondrial membrane potential(MMP),and the destruction of the balance of mitochondrial dynamic and micromorphology.Furthermore,there was a marked increase in reactive oxygen species(ROS),which led to oocyte lipid peroxidation(LPO).PS-NPs exposure induced abnormal intracellular iron overload,and subsequently increased the expression of transferrin receptor(TfRC),solute carrier family 7 member 11(SLC7a11),and acyl-CoA synthetase long-chain family member 4(ACSL4),which resulted in ferroptosis in oocytes.PS-NPs also indu ced oocyte maturation failure,cytoskeletal dysfunction and DNA damage.Cotreatment with 5μmol/L ferrostatin-1(Fer-1,an inhibitor of ferroptosis)alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation.Conclusions In conclusion,PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism,leading to the failure of oocyte maturation.
文摘With indica ( Oryza sativa L.) hybrid Shanyou 63 as control, the hybrid rice varieties including Peiai 64S/E32, Peiai 64S/9311, X07S/Zihui 100, Guangyou 881 and japonica 9516 were used to study changes of chlorophyll content, photosynthetic response to light intensity and temperature, chlorophyll fluorescence characteristics and membrane lipid peroxidation in their flag leaves at the late stage of development under natural conditions in Nanjing. The results were as follows:. primary photochemical efficiency of PS II ( F-v / F-m), quantum yield of linear electron transport of PS II (phi(PSII)), electron transfer rate (ETR) in these rice varieties decreased with their decrease of chlorophyll content during this period. This kind of impediment to energy conversion induced the transfer of excessive energy to the reducing side of PS I, hence the accumulation of O-2(radical anion) and peroxidation of membrane lipid, and resulting in the accumulation of malondialdehyde (MDA), that is the destroys of photosynthetic pigments and membranes and the consequent, premature senescence. This phenomenon is variable conspicuously in different rice varieties. Under natural condition in Nanjing, F-v/F-m, phi(PSII), ETR and quenching coefficient ( qP) in japonica 9516 tolerant to photooxidation decreased less and the conversion capacity of light energy was stable, premature senescence was unlikely, and consequently the seed-setting rate was higher. While F-v/F-m, phi(PSII), ETR and photochemical qP in Shanyou 63 sensitive to photooxidation decreased more and therefore premature senescence was easy to happen, thus the seed-setting rate and yield were all reduced. The tolerance to photooxidation and premature senescence in other hybrids derived from typical two line or three line crossing laid in the middle. From the rice breeding for super-high-yield, on the basis of the good plant-type of current rice, considering both hybrid vigor and the prevention premature senescence, it would be a notable strategy to use japonica maternal line or maternal. lines with some japonica genotype as the sterile lines in rice breeding.
基金Supported by the Foundation of State Developing and ReformingCommittee(No.IFZ20051210)the National Natural Science Foundationof China(No.30570323,No.20471030)the Programsin Science and Technology of Nantong(No.DE2009006,No.S2009019)~~
文摘[ Objective] The aim was to provide strategies for development of rare earth and control of environmental pollution. [ Method] Responses of membrane lipid peroxidation and endogenous hormones of soybean seedlings to UV-B radiation and rare earth were studied through hydroponics in laboratory. [ Result] The results showed that under irradiation of UV-B（ T1-0.15 W/m^2 and T2-0.45 W/m^2）, chlorophyll and indole-3-acetic acid（IAA） contents firstly decreased during the stress phase （1 -5 d） and then increased during the restoration phase （6 -9 d） while contents of malonadialdehyde（MDA） and abscisic acid（ABA） gradually increased during the imposition of UV-B radiation （1 -5 d） and subsequently decreased during recovery from UV-B stress （6 -9 d） . With adding of La （III） with the concentration of 20 mg · L^-1 , the decline/dse trend of chlorophyll, IAA, MDA and ABA contents was slowed down during the stress period while the rise/decline speed was accelerated during the recovery period. [ Conclusion] It suggests that the regulation of La （ III ） on membrane lipid peroxidation and endogenous hormones could increase chlorophyll and IAA contents, improve the metabolism of reactive oxygen species （ ROS）, inhibit membrane lipid peroxidation, decrease the accumulation amount of ABA and alleviate injury of UV-B radiation to soybean seedlings. Further, the protective potential of La （ III ） was better under low UV-B radiation than under high one.
文摘AIM To study the protective effects of tea polyphenol (TP) on cerebral ischemia reperfusion injury in rats and its scavenging oxygen free radical(OFR) activities and antilipid peroxidation in vitro . METHODS Cerebral ischemia reperfusion injury was produced by bilateral ligation of the common carotid arteries with vagus nerves and reperfusion for 45 min. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. Superoxide anion (O 2) from xanthine xanthine oxidase system and hydroxyl radical (·OH) from Fe 2+ -H 2O 2 system were determined with spectrophotometry. RESULTS During Cerebral ischemia reperfusion,TP improved the activities of superoxide dismutase ( P 【0 05), GSH peroxidase( P 【0 01) and catalase( P 【0 01), while decreasing the maiondialdchyde content in the brain( P 【0 05) and brain water content ( P 【0 01). Tea polyphenol possessed significantly scavenging effects on ·OH produced by Fenton reaction and O 2 produced by xanthine xanthine oxidase system (the IC 50 were 2 2 mmol·L -1 and 1 9 mmol·L -1 respectively). Tea polyphenol could significant inhibit the lipid peroxidation of cerbral mitochondrial membrane induced by ·OH in a concentration dependent manner. CONCLUSION The results indicate that tea polyphenol could protect the injury on cerebral ischemia reperfusion in rats for OFR, these effects may be related to its scavenging effects on oxygen free radicals and antilipid peroxidant.
文摘The effect of weak light on the peroxidation of membrane_lipid of one_year_old cherries ( Prunus pseudocerasus L. 'Laiyang') was studied by whole_tree shading. The results showed that the net photosynthetic rate of cherry leaves under weak light was remarkably lower; the activity peroxidase (POD) increased when light intensity decreased; the activity of catalase (CAT) showed an opposite trend, and it was positively correlated with light intensity; the activity of superoxide dismutase (SOD) increased under 366 μmol·m -2 ·s -1 and 533.8 μmol·m -2 ·s -1 light intensity, but decreased under 228.8 μmol·m -2 ·s -1 and 83.9 μmol·m -2 ·s -1 light intensity. A remarkable increase of malondialdehyde (MDA), a product of membrane_lipid peroxidation, was also observed in cherry leaves when treated with weak light, indicating more serious peroxidation in the membrane.
文摘Relationships between fluorescence parameters and membrane lipid peroxidation in leaves of indica and japonica rice (Oryza sativa L.) during later growth stage were studied under chilling temperature and strong light stress conditions. Results showed that D1 protein contents of PSⅡ in photosynthetic apparatus dropped, the generation of antheraxanthin (A) and zeaxanthin (Z) of xanthophyll cycle were inhibited partly, PSⅡ photochemical efficiency (F v/F m)and non-photochemical quenching (q N) were also decreased obviously. In addition, endogenous active oxygen scavenger—superoxide dismutase (SOD) reduced, superoxide anion radical (O -· 2) and malondialdehyde (MDA) accumulated, as a result, photooxidation of leaves occurred under chilling temperature and strong light stress conditions. Obvious differences in the changes of the above mentioned physiological parameters between indica and japonica rice were observed. Experiments in leaves treated with inhibitors under chilling temperature and strong light conditions showed that indica rice was more sensitive to chilling temperature with strong light and subjected to photooxidation more than japonica rice. Notable positive correlation between D1 protein contents and F v/F m or (A+Z)/(A+Z+V), and a marked negative correlation between F v/F m and MDA contents were obtained by regression analysis in indica and japonica rice during chilling temperature and strong light conditions. According to the facts mentioned above, it was inferred that PSⅡ photochemical efficiency(F v/F m) was the key index to forecast for the prediction of photooxidation under stress circumstances and the physiological basis were the synthetic capacity of D1 protein and the protection of xanthophyll cycle.
文摘Using various high-yield rices (Oryza sativa L.) such as japonica cultivar 9516, two parental line hybrid rice between subspecies with more japonica element Peiai 64/E32, Liangyoupeijiu (Peiai 64/9311), and indica hybrid rices X07S/Zihui 100, Gangyou 881, Shanyou 63 as the materials, the characteristics of chlorophyll fluorescence and membrane-lipid peroxidation of detached leaves at booting stage under photooxidation conditions were studied. In comparison with indica hybrid rice, after the photooxidation treatment, the primary photochemical efficiency of PS II (F-v/F-m), quantum yield of linear electron transport of PS II (Phi(PSII)) and photochemical quenching coefficient (qP) in japonica cultivar and hybrid rice with japonica decreased less. This indicated that high-yield rice with japonica was able to maintain higher capability of light energy conversion, resulting in the alleviation of photoinhibition. Meanwhile, the higher activities of protective enzymes such as superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) led to the less accumulation of endogenous active oxygen (O-(2)(radical anion), H2O2) and less content of the malondialdehyde (MDA) and the less decline of chlorophyll and protein contents, indicating a stronger tolerance to photooxidation. The changes in contents of chlorophyll and protein among various nee cultivars during photooxidation treatment were consistent with the decline of chlorophyll content from heading stage to maturation stage under natural conditions. Statistical analysis showed that there was a significant correlation between the indexes of tolerance to photooxidation and the rate of seed setting, implying that the cultivar tolerated to photooxidation had higher resistance to early aging of leaf. These results suggested that from a view of superhigh-yield breeding, considering both the utilization of heterosis and the resistance to early aging of leaf, introduction of japonica element tolerating to photooxidation into the rice sterile line (maternal plant) is a breeding strategy worthy to pay great attention to.
基金Supported by National Natural Science Foundation of China(No.30671061)Natural Science Foundation of Shanxi Province(No.2008011059-1 and No.20041101)~~
文摘[Objective] Effects of different concentrations of nitric oxide on membrane lipid peroxidation of wheat induced by enhanced UV-B radiation were researched,sodium nitroprusside （SNP） was selected as an exogenous nitric oxide（NO）donor.[Method] There are 3 groups including CK,UV treatment group （B）,B＋SNP treatment group,0,1,2,3,4 d sampling after treatment respectively,and physiological and biochemical indexes of MDA content and CAT,POD,SOD and so on were determined,repeated 3 times,and statistical analyzed.[Result] The results showed that,after the enhanced UV-B radiation,activity of the catalase （CAT）,superoxide dismutase （SOD） and of the guaiacol peroxidase （POD） all reduced apparently,and the concentration of malondialdehyde （MDA） increased obviously,leading to oxidative damage in wheat seedlings.Impose different concentrations of SNP after UV-B radiation,may mitigate oxidative damage of wheat seedling from different degrees,which was in agreement with the effect of making the concentration of MDA decrease and the activity of the CAT,SOD and POD all increased.The mitigation role of 0.01 mol/L SNP was more obvious for roots＇ oxidative damage,while 0.1 mmol/L SNP is more effective for oxidative damage of leaves.[Conclusion] Exogenous NO donor SNP had obvious relieve effects on oxidative damage of wheat seedlings caused by UV-B radiation,which can enhance adaptive capacity of plants to adversity stress.
基金The item of scieace and technology research plans of Zhejiang Province (No 1999-2-121)
文摘AIM:To study relationship of injury induced by nitric oxide, oxidation, peroxidation,lipoperoxidation with chronic cholecystitis.METHODS:The values of plasma nitric oxide (P-NO), plasma vitamin C (P-VC), plasma vitamin E (P-VE), plasma beta-carotene (P-beta-CAR), plasma lipoperoxides (P-LPO), erythrocyte superoxide dismutase (E-SOD), erythrocyte catalase (E-CAT), erythrocyte glutathione peroxidase (E-GSH-Px) activities and erythrocyte lipoperoxides (E-LPO) level in 77 patients with chronic cholecystitis and 80 healthy control subjects were determined, differences of the above average values between the patient group and the control group and differences of the average values between preoperative and postoperative patients were analyzed and compared, linear regression and correlation of the disease course with the above determination values as well as the stepwise regression and correlation of the course with the values were analyzed.RESULTS:Compared with the control group, the average values of P-NO, P-LPO, E-LPO were significantly increased (P【0.01), and of P-VC, P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px decreased (P 【0.01) in the patient group. The analysis of the linear regression and correlation showed that with prolonging of the course, the values of P-NO, P-LPO and E-LPO in the patients were gradually ascended and the values of P-VC,P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px descended (P【0.01). The analysis of the stepwise regression and correlation indicated that the correlation of the course with P-NO, P-VE and P-beta-CAR values was the closest. Compared with the preoperative patients, the average values of P-NO, P-LPO and E-LPO were significantly decreased (P 【0.01) and the average values of P-VC, E-SOD, E-CAT and E-GSH-Px in postoperative patients increased (P 【0.01) in postoperative patients. But there was no significant difference in the average values of P-VE, P-beta-CAR preoperative and postoperative patients.CONCLUSION:Chronic cholecystitis could induce the increase of nitric oxide, oxidation, peroxidation and lipoperoxidation.
文摘[ Objective] The aim of this study was to discuss the effect of antioxidants and lipid peroxidation from pea crops of plateau. [ Method] SOD enzyme liquid from pea crops of plateau was extracted by means of protein concentration assay, enzyme activity assay and antioxidant activity determination by DPPH method, peroxide activity inhibition of in vitro tissues from mice by homogenate MDA colorimetry method and lipid peroxidation assay of in vitro tissues. [ Result ] IC50 of the crude enzyme liquid extracted from pea on DPPH was 55.16 mg/L, while the scavenging rate of the crude enzyme liquid was lower than that of ascorbic acid, tea polyphenol and citric acid with the same concentration. The synergistic effect was found in ascorbic acid and crude enzyme liquid, but the synergism of ascorbic acid was better than that of citric acid. IC50 of SOD enzyme liquid extracted from pea on DPPH was 11.1 mg/L, which was better than that of tea polyphenol and closely similar to that of ascorbic acid. SOD enzyme liquid extracted from pea had an inhibitory effect on MDA production from in vitro tissues such as liver, kidney and heart, especially for a significantly inhibitory effect on MDA from liver in vitro. When the concentration was 0.25 mg/ml, the inhibition rate reached 78.3%, and then the inhibition rate increased little with the concentration incresas, while its effect on heart and kidney were inferior. [ Conclusion] SOD crude enzyme liquid and SOD enzyme liquid extracted from pea all have certain DPPH scavenging capacity, while SOD enzyme liquid extracted from pea has an inhibitory effect on lipid peroxidation.
基金Supported by a grant for young researcher from Ministry of Public Health of P.R.C.
文摘The main purpose of this study was to investigate the protective actions of captopril and cicaprost on changes of membrane fluidity of cultured neonatal rat myocardial cells exposed to anoxia and sugar deprivation.Lipid peroxidation level estimated by determining the thiobarbituric acid reactive substance(TBARS)content and lactate dehydrogenase(LDH)released in culture medium was also observed in order to examine other membrane-related changes due to anoxia.Membrane fluidity was monitored by measuring changes in the steady state fluorescence anisotropy(r_s)by fluorescence spectroscopy.The r_s value,TBARS level and LDH release were significantly increased after 3 h anoxia.Captopril(180 μmol/L),cicaprost(30 nmol/L)and indomethacin(1μmol/L)did not alter r_s, TBARS level and LDH activity of normal cultured neonatal rat myocardial cells.However,both captopril and cicaprost significantly prevented the increases of r_s,TBARS content and LDH release in those cells exposed to anoxia and sugar deprivation.lndomethacin abolished the actions of captopril on TBARS production and LDH release,but maintained its membrane fluidity protection.These results indicate that captopril and cicaprost protect membrane fluidity and lipid peroxidation changes in anoxia- injured myocardial cells.The action mechanism of captopril may be due,in part,to stimulation of prostacyclin synthesis and/or release.
文摘The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe 2+ were tested by differential spectrum. Superoxide anion (O 2)from xanthine xanthine oxidase (Xan XO) system and hydroxyl radical (·OH) from FeSO 4 H 2O 2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan XO and FeSO 4 H 2O 2 system. The IC 50 of Bre were 93 01 μmol·L -1 for Xan XO system and 62 18 μmol·L -1 for FeSO 4 H 2O 2 system. Bre also scavenged O 2 and ·OH produced by Xan XO and FeSO 4 H 2O 2 systems. The IC 50 of Bre were 32 63 μmol·L -1 for O - 2 and 20 22 μmol·L -1 for ·OH. Furthermore, the chelating Fe 2+ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe 2+ and scavenging O 2 as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.
