Does Ataxia Telangiectasia Mutated (ATM) protect testicular and germ cell DNA integrity by regulating the redox status?

Roger W. L. Godschalk*, Kimberly Vanhees, Ludovicus Maas, Marie Jose Drittij - Reijnders, Danielle Pachen, Sahar van Waalwijk van Doorn-Khosrovani, Frederik J. van Schooten, Guido R. M. M. Haenen

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


A balanced redox homeostasis in the testis is essential for genetic integrity of sperm. Reactive oxygen species can disturb this balance by oxidation of glutathione, which is regenerated using NADPH, formed by glucose-6-phosphate dehydrogenase (G6PDH). G6PDH is regulated by the Ataxia Telangiectasia Mutated (Atm) protein. Therefore, we studied the redox status and DNA damage in testes and sperm of mice that carried a deletion in Atm. The redox status in heterozygote mice, reflected by glutathione levels and antioxidant capacity, was lower than in wild type mice, and in homozygotes the redox status was even lower. The redox status correlated with oxidative DNA damage that was highest in mice that carried Atm deletions. Surprisingly, G6PDH activity was highest in homozygotes carrying the deletion. These data indicate that defective Atm reduces the redox homeostasis of the testis and genetic integrity of sperm by regulating glutathione levels independently from G6PDH activity.
Original languageEnglish
Pages (from-to)169-173
JournalReproductive Toxicology
Publication statusPublished - Aug 2016


  • Ataxia Telangiectasia Mutated
  • DNA damage
  • Oxidative stress
  • Testis
  • Glutathione
  • Glucose-6-phosphate dehydrogenase

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