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Since mitochondrial function is frequently defective in populations of human spermatozoa [56], it is possible that this trans-plasma membrane redox system is up-regulated in defective human spermatozoa in a similar fashion to the enhanced activity recorded in Rho O cells in order to maintain the redox status of the NAD + /NADH couple

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10.1074/jbc.M109.018911 J

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Antioxidants targeting mitochondrial oxidative stress: Promising neuroprotectants for epilepsy