The oxidation behavior of 316L austenitic steel after thermal aging process at 600℃for 6 h was investigated in the supercritical water(600℃/25 MPa)with 1000 h.Results showed that the grain size and the proportion of...The oxidation behavior of 316L austenitic steel after thermal aging process at 600℃for 6 h was investigated in the supercritical water(600℃/25 MPa)with 1000 h.Results showed that the grain size and the proportion of high angle grain boundaries(HAGB)increased in the steel after thermal aging process,with the observation of micro-textures.The weight gain rate of the steel after aging process increased,presenting the decreased Cr_(2)O_(3)contain in the oxide layer,which resulted in the increasing diffusion rate of Fe and O ions in oxide layer.The molecular dynamics simulation results confirmed the high oxidation rate in HAGB and micro-textures for the 316L steel after aging process.展开更多
As a widely used plasticizer,di-(2-ethylhexyl)phthalate(DEHP)is known to induce significant testicular injury.However,the potential mechanism and effects of pubertal exposure to DEHP on testis development remain uncle...As a widely used plasticizer,di-(2-ethylhexyl)phthalate(DEHP)is known to induce significant testicular injury.However,the potential mechanism and effects of pubertal exposure to DEHP on testis development remain unclear.In vivo,postnatal day(PND)21 male rats were gavaged with 0,250,and 500 mg/kg DEHP for ten days.Damage to the seminiferous epithelium and disturbed spermatogenesis were observed after DEHP exposure.Meanwhile,oxidative stress-induced injury and pyroptosis were activated.Both endoplasmic reticulum(ER)stress and mitophagy were involved in this process.Monoethylhexyl phthalate(MEHP)was used as the biometabolite of DEHP in vitro.The GC-1 and GC-2 cell lines were exposed to 0,100μM,200μM,and 400μM MEHP for 24 h.Reactive oxygen species(ROS)generation,oxidative stress damage,ER stress,mitophagy,and pyroptosis were significantly increased after MEHP exposure.The ultrastructure of the ER and mitochondria was destroyed.X-box binding protein 1(XBP1)was observed to be activated and translocated into the nucleus.ROS generation was inhibited by acetylcysteine.The levels of antioxidative stress,ER stress,mitophagy,and pyroptosis were decreased as well.After the administration of the ER stress inhibitor 4-phenyl-butyric acid,both mitophagy and pyroptosis were inhibited.Toyocamycin-induced XBP1 down-regulation decreased the levels of mitophagy and pyroptosis.The equilibrium between pyroptosis and mitophagy was disturbed by XBP1 accumulation.In summary,our findings confirmed that DEHP induced a ROS-mediated imbalance in pyroptosis and mitophagy in immature rat testes via XBP1.Moreover,XBP1 might be the key target in DEHP-related testis dysfunction.展开更多
基金supported by the Hebei Natural Science Foundation(E2023502105)the China Postdoctoral Science Foundation(2023M741155)the Fundamental Research Funds for the Central Universities(JB2023030).
文摘The oxidation behavior of 316L austenitic steel after thermal aging process at 600℃for 6 h was investigated in the supercritical water(600℃/25 MPa)with 1000 h.Results showed that the grain size and the proportion of high angle grain boundaries(HAGB)increased in the steel after thermal aging process,with the observation of micro-textures.The weight gain rate of the steel after aging process increased,presenting the decreased Cr_(2)O_(3)contain in the oxide layer,which resulted in the increasing diffusion rate of Fe and O ions in oxide layer.The molecular dynamics simulation results confirmed the high oxidation rate in HAGB and micro-textures for the 316L steel after aging process.
基金supported by the National Natural Science Foundation of China(No.81771566,82071632)the Postgraduate Research Innovation Project of Chongqing Medical University(China)(No.CYB22210)the Youth Basic Research Project from the Ministry of Education Key Laboratory of Child Development and Disorders(China)(No.YBRP-202114).
文摘As a widely used plasticizer,di-(2-ethylhexyl)phthalate(DEHP)is known to induce significant testicular injury.However,the potential mechanism and effects of pubertal exposure to DEHP on testis development remain unclear.In vivo,postnatal day(PND)21 male rats were gavaged with 0,250,and 500 mg/kg DEHP for ten days.Damage to the seminiferous epithelium and disturbed spermatogenesis were observed after DEHP exposure.Meanwhile,oxidative stress-induced injury and pyroptosis were activated.Both endoplasmic reticulum(ER)stress and mitophagy were involved in this process.Monoethylhexyl phthalate(MEHP)was used as the biometabolite of DEHP in vitro.The GC-1 and GC-2 cell lines were exposed to 0,100μM,200μM,and 400μM MEHP for 24 h.Reactive oxygen species(ROS)generation,oxidative stress damage,ER stress,mitophagy,and pyroptosis were significantly increased after MEHP exposure.The ultrastructure of the ER and mitochondria was destroyed.X-box binding protein 1(XBP1)was observed to be activated and translocated into the nucleus.ROS generation was inhibited by acetylcysteine.The levels of antioxidative stress,ER stress,mitophagy,and pyroptosis were decreased as well.After the administration of the ER stress inhibitor 4-phenyl-butyric acid,both mitophagy and pyroptosis were inhibited.Toyocamycin-induced XBP1 down-regulation decreased the levels of mitophagy and pyroptosis.The equilibrium between pyroptosis and mitophagy was disturbed by XBP1 accumulation.In summary,our findings confirmed that DEHP induced a ROS-mediated imbalance in pyroptosis and mitophagy in immature rat testes via XBP1.Moreover,XBP1 might be the key target in DEHP-related testis dysfunction.
