Aflatoxin B1 Disrupts Ovarian Follicular Dynamics and Activates Intrinsic Apoptosis-Related Signaling in Rat Ovaries: Interactions Between Hormonal Imbalance and Follicular Atresia.

BACKGROUND

Aflatoxin B1 (AFB1) is one of the most potent naturally occurring mycotoxins and has been implicated in reproductive toxicity. The present study is aimed at evaluating the time-dependent effects of experimental AFB1 exposure on ovarian follicular dynamics, reproductive hormone profiles, and intrinsic apoptosis-related markers in female rats.

METHODOLOGY: Twenty-four mature female Wistar rats were assigned to control and AFB1-exposed groups (N = 6 per time point). AFB1 was administered intraperitoneally at 20 mg/kg body weight for 7, 14, and 21 days. Ovarian tissue and serum samples were collected at the end of each designated exposure period. Follicular population and atresia were evaluated histologically; serum concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, and progesterone were measured by ELISA, and the expression patterns of Bcl-2, Bax, p53, and caspase-3 were assessed using RT-PCR and immunohistochemistry.

RESULTS

AFB1 exposure was associated with a time-dependent reduction in total follicular population and a marked increase in follicular atresia. Serum FSH, LH, estrogen, and progesterone concentrations were significantly decreased in AFB1-exposed animals compared with controls. At the molecular level, AFB1 decreased Bcl-2 expression while increasing Bax, p53, and caspase-3 expression in ovarian tissue, with prominent immunoreactivity in follicular cells.

CONCLUSION

These findings indicate that experimental AFB1 exposure is associated with impaired follicular development, endocrine disruption, and activation of intrinsic apoptosis-related signaling in rat ovaries. The observed coordinated changes suggest a biologically plausible interaction between hormonal imbalance and apoptosis-associated pathways in AFB1-induced follicular atresia, although functional validation is required to confirm direct causal mechanisms.