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In studies of GPX5 knockout mice, we deduced that GPX5 is a way to maintain the integrity of sperm DNA function by removing excess H 2 O 2 , and these mice did not exhibit significant defects in the epididymis and sperm cells ( 2 O 2 scavengers was detected (Noblanc et al., 2012), proving that after SNGPX4 and GPX5 double knockouts, the epididymal tissues of mice produced oxidative stress responses, indicating that SNGPX4 and GPX5 play a role in maintaining the normal structure of the sperm nucleus in the epididymal tissue (Noblanc et al., 2012)
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We observed that NB standard-of-care chemotherapy can interfere with certain ferroptosis-inducing mechanisms, particularly those targeting GPX4, and that the combination of ferroptosis-inducing drugs with current clinical therapy should be based on MOA
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