BioMed research international · 2026
Aflatoxin B1 Disrupts Ovarian Follicular Dynamics and Activates Intrinsic Apoptosis-Related Signaling in Rat Ovaries: Interactions Between Hormonal Imbalance and Follicular Atresia.
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Poursadeghi Farbod, Razi Mazdak, Amniattalab Amir
Аннотация
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.
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.