Background Mitochondrial dysfunction induced by excessive mitochondrial reactive oxygen species(ROS)damages embryonic development and leads to growth arrest.Objective The purpose of this study is to elucidate whether ...Background Mitochondrial dysfunction induced by excessive mitochondrial reactive oxygen species(ROS)damages embryonic development and leads to growth arrest.Objective The purpose of this study is to elucidate whether maternal zinc(Zn)exert protective effect on oxidative stress targeting mitochondrial function using an avian model.Result In ovo injected tert-butyl hydroperoxide(BHP)increases(P<0.05)hepatic mitochondrial ROS,malondialdehyde(MDA)and 8-hydroxy-2-deoxyguanosine(8-OHdG),and decreases(P<0.05)mitochondrial membrane potential(MMP),mitochondrial DNA(mtDNA)copy number and adenosine triphosphate(ATP)content,contributing to mitochondrial dysfunction.In vivo and in vitro studies revealed that Zn addition enhances(P<0.05)ATP synthesis and metallothionein 4(MT4)content and expression as well as alleviates(P<0.05)the BHP-induced mitochondrial ROS generation,oxidative damage and dysfunction,exerting a protective effect on mitochondrial function by enhancing antioxidant capacity and upregulating the mRNA and protein expressions of Nrf2 and PGC-1α.Conclusions The present study provides a new way to protect offspring against oxidative damage by maternal Zn supplementation through the process of targeting mitochondria involving the activation of Nrf2/PGC-1αsignaling.展开更多
基金sponsored by the National Key R&D Program of China(2022YFD1301800 and1300400)National Natural Science Foundation of China(31802080 and 3197200131)+1 种基金Key Open Laboratory of Chinese Veterinary Medicine of State Ethnic Affairs Commission&National Local Joint Engineering Research Centre for the Separation and Purification Technology of Ethnic Chinese Veterinary Medicine([2022]09)Guangdong Provincial Science and Technology Special Foundation(210723106900762 and 2021020103-2)。
文摘Background Mitochondrial dysfunction induced by excessive mitochondrial reactive oxygen species(ROS)damages embryonic development and leads to growth arrest.Objective The purpose of this study is to elucidate whether maternal zinc(Zn)exert protective effect on oxidative stress targeting mitochondrial function using an avian model.Result In ovo injected tert-butyl hydroperoxide(BHP)increases(P<0.05)hepatic mitochondrial ROS,malondialdehyde(MDA)and 8-hydroxy-2-deoxyguanosine(8-OHdG),and decreases(P<0.05)mitochondrial membrane potential(MMP),mitochondrial DNA(mtDNA)copy number and adenosine triphosphate(ATP)content,contributing to mitochondrial dysfunction.In vivo and in vitro studies revealed that Zn addition enhances(P<0.05)ATP synthesis and metallothionein 4(MT4)content and expression as well as alleviates(P<0.05)the BHP-induced mitochondrial ROS generation,oxidative damage and dysfunction,exerting a protective effect on mitochondrial function by enhancing antioxidant capacity and upregulating the mRNA and protein expressions of Nrf2 and PGC-1α.Conclusions The present study provides a new way to protect offspring against oxidative damage by maternal Zn supplementation through the process of targeting mitochondria involving the activation of Nrf2/PGC-1αsignaling.
