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Remarkably, paternal alcohol use appears to interact with maternal exposures to accelerate these mitochondrial deficits, promoting a sustained pro-inflammatory state, which increases offspring susceptibility to liver disease and hepatocellular carcinoma ( Our ongoing research indicates that chronic paternal alcohol consumption impairs mitochondrial function within the male reproductive tract, correlating with alterations in sperm noncoding RNAs and long-lasting changes in offspring mitochondrial activity ( Antioxidant therapies aim to mitigate oxidative stress, a condition characterized by an imbalance between reactive oxygen species and the cellular antioxidant defense ( Although healthy men commonly use antioxidants through their widespread incorporation into multivitamins and dietary supplements, in the absence of oxidative stress, this indiscriminate use may induce significant epigenetic alterations in the male germline, raising clinical and public health concerns ( N-acetyl-L-cysteine (NAC) and selenium (Se) are two widely studied antioxidant compounds used to investigate cellular responses to oxidative stress

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varies in different disease states, e.g., Lachnoclostridium spp