Tetrachloro-1,4-benzoquinone disrupts oocyte quality through mitochondrial dysfunction and oxidative stress.

Disinfection byproducts (DBPs) are emerging environmental contaminants with potential reproductive toxicity; however, the effects of tetrachloro-1,4-benzoquinone (TCBQ) on female fertility remain poorly understood. Using a mouse exposure model integrated with ovarian histological analysis, oocyte maturation assays, mitochondrial functional assessment, oxidative stress evaluation, and transcriptomic profiling, we investigated how TCBQ exposure affects follicular development and oocyte competence in pubertal female mice. TCBQ-exposed oocytes displayed abnormal spindle assembly and chromosome misalignment accompanied by mitochondrial dysfunction and early apoptosis. Transcriptomic analysis revealed a significant dysregulation of oxidative phosphorylation and antioxidant defense pathways in TCBQ-treated oocytes. Notably, co-treatment with melatonin reduced reactive oxygen species (ROS) accumulation, restored adenosine triphosphate (ATP) levels, and rescued meiotic progression. Melatonin supplementation partially rescued TCBQ-induced oocyte defects, with reduced oxidative stress and improved mitochondrial function. Collectively, these findings identify TCBQ as a potential reproductive toxicant that impairs oocyte competence through oxidative stress-associated mitochondrial dysfunction and meiotic disruption.