Aflatoxin B1 impairs spermatogenesis: An experimental study for crosslink between oxidative stress and mitochondria-dependent apoptosis.

The present experimental study was carried out to investigate the crosslink between aflatoxin B1 (AFB1)-induced oxidative stress and mitochondria-dependent apoptosis in testicles. For this purpose, 24 mature male Swiss albino mice were randomly divided into control and test groups. The AFB1 was dissolved in corn oil and ethanol (95:5, v/v) vehicle. The animals in test group subdivided into three groups, which received the AFB1 at a daily dose of 20 μg/kg body weight, through intraperitoneal (i.p.) route, for 7, 14, and 21 days. The mice in the control group received the vehicle alone for 21 days. The expression of Bcl-2, Bax, p53, and caspase-3 at both mRNA and protein levels were analyzed by using reverse transcription PCR (RT-PCR) and immunohistochemistry, respectively. Moreover, the mitochondrial content of germinal epithelium, tubular differentiation (TDI), and spermiogenesis (SPI) indices was analyzed. Finally, the apoptosis was assessed by using TUNEL staining. Observations revealed that the AFB1 remarkably (P < .05) reduced Bcl-2 expression at both mRNA and protein levels. Up-regulated Bax, caspase-3, and p53 expression were revealed in AFB1-received animals, which developed time-dependently. Histological examinations exhibited a significant reduction in TDI and SPI indices. Finally, the AFB1-induced apoptosis index increased time-dependently. In conclusion, the AFB1 adversely affects the spermatogenesis via inducing oxidative stress, diminishing cellular mitochondrial content and enhancing pro-apoptotic Bax, caspase-3, and p53 expression. All these impairments result in mitochondria-dependent apoptosis.