Does Ataxia Telangiectasia Mutated (ATM) protect testicular and germ cell DNA integrity by regulating the redox status?
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- 作者：Roger W.L. Godschalk ; r.godschalk@maastrichtuniversity.nl" class="auth_mail" title="E-mail the corresponding author ; Kimberly Vanhees1 ; Lou Maas ; Marie-Jose Drittij ; Danië ; lle Pachen ; Sahar van Waalwijk van Doorn-Khosrovani ; Frederik J. van Schooten ; Guido R.M.M. Haenen
- 关键词：Ataxia Telangiectasia Mutated ; DNA damage ; Oxidative stress ; Testis ; Glutathione ; Glucose-6-phosphate dehydrogenase
- 刊名：Reproductive Toxicology
- 出版年：2016
- 出版时间：August 2016
- 年：2016
- 卷：63
- 期：Complete
- 页码：169-173
- 全文大小：617 K
文摘
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The redox status in mice that carry at least one Atm-ΔSRI allele, reflected by glutathione levels and antioxidant capacity, was lower than in wild type mice.
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Glucose-6-phosphate dehydrogenase activity was higher in mice that were homozygous for Atm-ΔSRI when compared to heterozygous mice.
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Oxidative DNA damage in testis and sperm was increased in mice that carried the Atm-ΔSRI allele.
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Defective Atm reduces redox homeostasis of the testis and genetic integrity of sperm by regulating glutathione levels.