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In ovarian tumor (OT) tissues, DHT enhances the binding of NRF2 to Keap1, resulting in potentiated ubiquitination and degradation of NRF2, thereby activating oxidative stress and exhibiting anti-tumor effects [102]
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For instance, the intricate link between PD etiology and mitochondrial dysfunction, frequently modulated by complex genetic factors (124), may impact ferroptosis susceptibility
Decreased butyrate production is also associated with elevated oxygen levels in the intestinal mucosa, increasing the risk of oxidative damage [150]
