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The recurring interplay of oxidative stress, inflammatory activation, and disrupted cellular signalling provides a unifying mechanistic framework linking renal, musculoskeletal, cutaneous, immunological, respiratory, gastrointestinal, and reproductive dysfunctions to those already described in cardiovascular, hepatic, and gonadal tissues ( Taken together, the current body of evidence suggests that supraphysiological androgen exposure disrupts endocrine regulation at multiple levelsfrom hypothalamic control to testicular cellular architecturethrough oxidative, mitochondrial, and epigenetic mechanisms ( To facilitate synthesis of the extensive narrative data presented in Sections 6 and 7, a summary table is provided below, integrating the major psychological and physical adverse effects associated with non-medical testosterone and anabolicandrogenic steroid use across organ systems ( Table 2 )

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Redox homeostasis genes modulate response to APR-246 in a p53-dependent and p53-independent manner Previous studies have characterized APR-246 as a modulator of redox homeostasis and inducer of ROS through depletion of key antioxidants, resulting in both p53-dependent and -independent cell death pathways such as ferroptosis [26,27,28,29]

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