Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity
© 2017 Elsevier B.V. and Mitochondria Research Society Humanin (HN) is an endogenous peptide that exerts cytoprotection against oxidative stress and apoptosis. We recently reported that Humanin analogue (HNG) pretreatment can reduce reactive oxygen species production in the heart subjected to ischem...
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th-cmuir.6653943832-583122018-09-05T04:22:33Z Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity Savitree Thummasorn Krekwit Shinlapawittayatorn Juthamas Khamseekaew Thidarat Jaiwongkam Siriporn C. Chattipakorn Nipon Chattipakorn Biochemistry, Genetics and Molecular Biology © 2017 Elsevier B.V. and Mitochondria Research Society Humanin (HN) is an endogenous peptide that exerts cytoprotection against oxidative stress and apoptosis. We recently reported that Humanin analogue (HNG) pretreatment can reduce reactive oxygen species production in the heart subjected to ischemia/reperfusion (I/R) injury via attenuating mitochondrial dysfunction. However, it is unclear if HNG has direct effects on mitochondrial function against oxidative stress. Thus, we sought to determine the effects of HNG on mitochondrial function under hydrogen peroxide (H2O2) induced oxidative stress in isolated cardiac mitochondria. We found that HNG has direct protective effects on cardiac mitochondrial function against H2O2induced oxidative stress through decreasing complex I activity. 2018-09-05T04:22:33Z 2018-09-05T04:22:33Z 2018-01-01 Journal 18728278 15677249 2-s2.0-85027396732 10.1016/j.mito.2017.08.001 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85027396732&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/58312 |
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Biochemistry, Genetics and Molecular Biology Savitree Thummasorn Krekwit Shinlapawittayatorn Juthamas Khamseekaew Thidarat Jaiwongkam Siriporn C. Chattipakorn Nipon Chattipakorn Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
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© 2017 Elsevier B.V. and Mitochondria Research Society Humanin (HN) is an endogenous peptide that exerts cytoprotection against oxidative stress and apoptosis. We recently reported that Humanin analogue (HNG) pretreatment can reduce reactive oxygen species production in the heart subjected to ischemia/reperfusion (I/R) injury via attenuating mitochondrial dysfunction. However, it is unclear if HNG has direct effects on mitochondrial function against oxidative stress. Thus, we sought to determine the effects of HNG on mitochondrial function under hydrogen peroxide (H2O2) induced oxidative stress in isolated cardiac mitochondria. We found that HNG has direct protective effects on cardiac mitochondrial function against H2O2induced oxidative stress through decreasing complex I activity. |
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Journal |
author |
Savitree Thummasorn Krekwit Shinlapawittayatorn Juthamas Khamseekaew Thidarat Jaiwongkam Siriporn C. Chattipakorn Nipon Chattipakorn |
author_facet |
Savitree Thummasorn Krekwit Shinlapawittayatorn Juthamas Khamseekaew Thidarat Jaiwongkam Siriporn C. Chattipakorn Nipon Chattipakorn |
author_sort |
Savitree Thummasorn |
title |
Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
title_short |
Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
title_full |
Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
title_fullStr |
Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
title_full_unstemmed |
Humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex I activity |
title_sort |
humanin directly protects cardiac mitochondria against dysfunction initiated by oxidative stress by decreasing complex i activity |
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2018 |
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https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85027396732&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/58312 |
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