Effects and mechanisms of aflatoxin B1 on oocytes and embryo development.

Aflatoxin B1 (AFB1), a ubiquitous environmental contaminant, poses substantial threats to animal reproductive health. This review thoroughly described the damage effects and summarized the potential mechanisms of AFB1 on reproductive health. Following metabolic activation by cytochrome P450 to form aflatoxin B1-8, 9-epoxide (AFBO), AFB1 disrupts cellular architecture and impairs mitochondrial function. This impairment manifests as suppressed mitochondrial biogenesis, diminished membrane potential, and induction of mitochondrial DNA mutations. Consequently, energy metabolism dysregulation and arrested development occur in oocytes, embryonic cells, granulosa cells, and ovarian somatic cells. AFB1-induced oxidative stress activates apoptotic pathways and perturbs epigenetic reprogramming, thereby disrupting oocyte meiotic progression and gene expression. Furthermore, AFB1 inhibits GPX4 expression, upregulates TFRC and ACSL4 expression, and promotes iron accumulation, collectively driving lipid peroxidation and triggering ferroptosis. This cascade ultimately impedes oocyte maturation and compromises embryonic developmental competence. This study provides novel insights into the reproductive toxicity of AFB1 and establishes a scientific foundation for developing effective preventative and therapeutic strategies.