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This persistent state, referred to as anabolic-steroidinduced hypogonadism (ASIH), has been attributed to prolonged suppression of hypothalamic GnRH signalling, desensitisation of pituitary gonadotropes, and potential structural or functional impairment of Leydig cells (79)

Thus, as far as mitochondrial oxidative stress homeostasis is concerned, mGSH is a vital factor maintaining mitochondrial function, controlling cell survival/death, and its depletion causes cell damage and facilitates cell death [57, 59]