The protective role of glutathione peroxidase in apoptosis induced by reactive oxygen species. Kayanoki, Y., Fujii, J., Islam, K. N., Suzuki, K., Kawata, S., Matsuzawa, Y., & Taniguchi, N. Journal of Biochemistry, 119(4):817–822, April, 1996. abstract bibtex Selenium-dependent glutathione peroxidase (GPx) plays a protective role in oxidative stress-induced apoptosis. In this study, we demonstrated that MDBK cells, a bovine renal epithelial cell line, exhibited internucleosomal DNA fragmentation characteristic of apoptotic cell death under selenium-deficient conditions with lower doses of hydrogen peroxide (H2O2) than under selenium-supplemented ones. This was due to a decreased amount of GPx in the cells under selenium-deficient conditions, because other antioxidative enzyme activities were not affected by the selenium supplementation. Cumene hydroperoxide also induced DNA fragmentation in selenium-deficient cells but no ladder formation was observed. Flow cytometric analysis showed that selenium-deficient cells were less capable of scavenging intracellular peroxides after exposure to exogenous H2O2 than selenium-supplemented ones. In contrast, there was no difference in viability between selenium-supplemented and non-supplemented cells in cell survival after exposure to menadione, which activates the electron transport system and increases intracellular superoxide radicals. Clofibrate, a peroxisomal proliferator and an inducer of catalase (CAT), partially protected both Se-deficient and Se-supplemented cells from exogenous H202. We concluded that selenium-deficient cells were more easily brought to apoptotic cell death by peroxides, but not by superoxide radicals, than selenium-supplemented ones and that CAT could compensate for the depletion of GPx to a certain degree by scavenging H2O2.
@article{kayanoki_protective_1996,
title = {The protective role of glutathione peroxidase in apoptosis induced by reactive oxygen species},
volume = {119},
issn = {0021-924X},
abstract = {Selenium-dependent glutathione peroxidase (GPx) plays a protective role in oxidative stress-induced apoptosis. In this study, we demonstrated that MDBK cells, a bovine renal epithelial cell line, exhibited internucleosomal DNA fragmentation characteristic of apoptotic cell death under selenium-deficient conditions with lower doses of hydrogen peroxide (H2O2) than under selenium-supplemented ones. This was due to a decreased amount of GPx in the cells under selenium-deficient conditions, because other antioxidative enzyme activities were not affected by the selenium supplementation. Cumene hydroperoxide also induced DNA fragmentation in selenium-deficient cells but no ladder formation was observed. Flow cytometric analysis showed that selenium-deficient cells were less capable of scavenging intracellular peroxides after exposure to exogenous H2O2 than selenium-supplemented ones. In contrast, there was no difference in viability between selenium-supplemented and non-supplemented cells in cell survival after exposure to menadione, which activates the electron transport system and increases intracellular superoxide radicals. Clofibrate, a peroxisomal proliferator and an inducer of catalase (CAT), partially protected both Se-deficient and Se-supplemented cells from exogenous H202. We concluded that selenium-deficient cells were more easily brought to apoptotic cell death by peroxides, but not by superoxide radicals, than selenium-supplemented ones and that CAT could compensate for the depletion of GPx to a certain degree by scavenging H2O2.},
language = {eng},
number = {4},
journal = {Journal of Biochemistry},
author = {Kayanoki, Y. and Fujii, J. and Islam, K. N. and Suzuki, K. and Kawata, S. and Matsuzawa, Y. and Taniguchi, N.},
month = apr,
year = {1996},
pmid = {8743587},
keywords = {Animals, Antioxidants, Apoptosis, Benzene Derivatives, Catalase, Cattle, Cell Line, Cell Survival, Clofibrate, Glucose Oxidase, Glutathione Peroxidase, Hydrogen Peroxide, Oxidative Stress, Peroxides, Reactive Oxygen Species, Selenious Acid, Selenium, Selenium Compounds, Superoxide Dismutase, Superoxides, Vitamin K, Xanthine Oxidase},
pages = {817--822},
}
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This was due to a decreased amount of GPx in the cells under selenium-deficient conditions, because other antioxidative enzyme activities were not affected by the selenium supplementation. Cumene hydroperoxide also induced DNA fragmentation in selenium-deficient cells but no ladder formation was observed. Flow cytometric analysis showed that selenium-deficient cells were less capable of scavenging intracellular peroxides after exposure to exogenous H2O2 than selenium-supplemented ones. In contrast, there was no difference in viability between selenium-supplemented and non-supplemented cells in cell survival after exposure to menadione, which activates the electron transport system and increases intracellular superoxide radicals. Clofibrate, a peroxisomal proliferator and an inducer of catalase (CAT), partially protected both Se-deficient and Se-supplemented cells from exogenous H202. We concluded that selenium-deficient cells were more easily brought to apoptotic cell death by peroxides, but not by superoxide radicals, than selenium-supplemented ones and that CAT could compensate for the depletion of GPx to a certain degree by scavenging H2O2.","language":"eng","number":"4","journal":"Journal of Biochemistry","author":[{"propositions":[],"lastnames":["Kayanoki"],"firstnames":["Y."],"suffixes":[]},{"propositions":[],"lastnames":["Fujii"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Islam"],"firstnames":["K.","N."],"suffixes":[]},{"propositions":[],"lastnames":["Suzuki"],"firstnames":["K."],"suffixes":[]},{"propositions":[],"lastnames":["Kawata"],"firstnames":["S."],"suffixes":[]},{"propositions":[],"lastnames":["Matsuzawa"],"firstnames":["Y."],"suffixes":[]},{"propositions":[],"lastnames":["Taniguchi"],"firstnames":["N."],"suffixes":[]}],"month":"April","year":"1996","pmid":"8743587","keywords":"Animals, Antioxidants, Apoptosis, Benzene Derivatives, Catalase, Cattle, Cell Line, Cell Survival, Clofibrate, Glucose Oxidase, Glutathione Peroxidase, Hydrogen Peroxide, Oxidative Stress, Peroxides, Reactive Oxygen Species, Selenious Acid, Selenium, Selenium Compounds, Superoxide Dismutase, Superoxides, Vitamin K, Xanthine Oxidase","pages":"817–822","bibtex":"@article{kayanoki_protective_1996,\n\ttitle = {The protective role of glutathione peroxidase in apoptosis induced by reactive oxygen species},\n\tvolume = {119},\n\tissn = {0021-924X},\n\tabstract = {Selenium-dependent glutathione peroxidase (GPx) plays a protective role in oxidative stress-induced apoptosis. In this study, we demonstrated that MDBK cells, a bovine renal epithelial cell line, exhibited internucleosomal DNA fragmentation characteristic of apoptotic cell death under selenium-deficient conditions with lower doses of hydrogen peroxide (H2O2) than under selenium-supplemented ones. This was due to a decreased amount of GPx in the cells under selenium-deficient conditions, because other antioxidative enzyme activities were not affected by the selenium supplementation. Cumene hydroperoxide also induced DNA fragmentation in selenium-deficient cells but no ladder formation was observed. Flow cytometric analysis showed that selenium-deficient cells were less capable of scavenging intracellular peroxides after exposure to exogenous H2O2 than selenium-supplemented ones. In contrast, there was no difference in viability between selenium-supplemented and non-supplemented cells in cell survival after exposure to menadione, which activates the electron transport system and increases intracellular superoxide radicals. Clofibrate, a peroxisomal proliferator and an inducer of catalase (CAT), partially protected both Se-deficient and Se-supplemented cells from exogenous H202. We concluded that selenium-deficient cells were more easily brought to apoptotic cell death by peroxides, but not by superoxide radicals, than selenium-supplemented ones and that CAT could compensate for the depletion of GPx to a certain degree by scavenging H2O2.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Journal of Biochemistry},\n\tauthor = {Kayanoki, Y. and Fujii, J. and Islam, K. 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