This research demonstrates that copper-induced cell death (cuproptosis) impairs female oocyte maturation by disrupting mitochondrial function and energy production. The study found that NMN supplementation—a NAD+ precursor—effectively restores mitochondrial function and partially rescues meiotic arrest in oocytes exposed to copper stress. The findings position NAD+ metabolism as a therapeutic target for protecting egg quality and female fertility, with direct clinical implications for practitioners working with reproductive health.
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NMN supplementation partially restored mitochondrial function in copper-stressed oocytes, suggesting NAD+ support may help preserve egg quality under oxidative stress.