Involvement of Pro- and Anti-Apoptotic Markers in Perfluorooctanoic Acid (PFOA) Induced Testicular Disruption in Wistar Rats
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Abstract
Perfluorooctanoic Acid (PFOA) induces reproductive toxicity in males by obstructing germ cell differentiation, increasing oxidative stress, and degrading vital intercellular junctions. While extensive research associates PFOA with testicular dysfunction and atrophy, its impact on pro- and anti-apoptotic factors remains less explored. The present study investigates the dose-dependent effects of PFOA on p53, caspase-3, and BCL2 to evaluate their potential impact on testicular growth. Four groups of Wistar male rats were studied: Group II received 2 mg/kg PFOA/day, Group III received 5 mg/kg PFOA/day, and Group IV received 10 mg/kg PFOA/day. Each group consisted of five rats treated for 45 days. A control group (Group I) of equal size was included for parallel comparison. The weights of the main and accessory reproductive organs were recorded. The expression of p53, BCL2, and caspase-3 in testicular tissues was assessed immunohistochemically to determine the impact of PFOA on testicular cell proliferation. The results indicated a sharp, dose-dependent decline in testicular and epididymal weight. The expression of p53 increased substantially in animals administered 10 mg/kg PFOA/day. Similarly, caspase-3 expression significantly increased in a dose-dependent manner, demonstrating a direct association with PFOA exposure. Conversely, BCL2 expression decreased markedly in animals treated with 10 mg/kg PFOA/day. These findings suggest a caspase-3-dependent cleavage of BCL2 and activation of p53 in the germ cells of PFOA-treated rats. In conclusion, the study demonstrates that the loss of testicular and epididymal weight in PFOA-administered rats is attributable to high apoptosis, ultimately leading to testicular atrophy.
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