MOTS-c is a mitochondrial-derived peptide that activates AMPK through direct mitochondrial signaling and nuclear translocation under metabolic stress, whereas metformin activates AMPK indirectly by inhibiting Complex I of the mitochondrial electron transport chain, and AICAR mimics AMP to trick the cell into AMPK activation
This phenomenon is further complicated by reported no observed adverse effect levels (NOAELs) that vary by 23 orders of magnitude across studies, likely reflecting differences in metabolic processing, genetic susceptibility, and methodological approaches ( 1.3 Objectives of this review This comprehensive review synthesizes current evidence (20192024) regarding EED-mediated reproductive toxicity in males, with particular emphasis on: Mechanistic Understanding: Elucidating the molecular pathways through which EEDs disrupt male reproductive function, including oxidative stress cascades, endocrine signaling interference, and epigenetic modifications
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