Nicotine-induced damages in testicular tissue of rats; evidences for bcl-2, p53 and caspase-3 expression.

OBJECTIVES

Present study was performed in order to uncover new aspects for nicotine-induced damages on spermatogenesis cell lineage.

MATERIALS AND METHODS

For this purpose, 36 mature male Wistar rats were divided into three groups as; control-sham (0.2 ml, saline normal, IP), low dose (0.2 mg/kg BW, IP) nicotine-received and high dose (0.4 mg/kg BW, IP) nicotine-received groups. Following 7 weeks, the expression of bcl-2, p53 and caspase-3 at mRNA and protein levels were investigated by using reverse-transcriptase PCR (RT-PCR) and immunohistochemical (IHC) analyses, respectively. Moreover, the serum level of FSH, LH and testosterone were evaluated. Finally, the mRNA damage was analyzed by using special fluorescent staining.

RESULTS

Nicotine, at both dose levels, decreased tubular differentiation, spermiogenesis and repopulation indices and enhanced cellular depletion. Animals in nicotine-received groups exhibited a significant (<0.05) reduction at mRNA and protein levels of bcl-2. More analyses revealed a remarkable (<0.05) enhancement in expression of p53 and caspase-3 in comparison to control-sham animals. Finally, nicotine resulted in a significant (<0.05) reduction in serum level of testosterone and elevated mRNA damage.

CONCLUSION

Our data showed that, nicotine by suppressing the testosterone biosynthesis, reducing mRNA and protein levels of bcl-2 and up regulating the p53 and caspase-3 mRNA and protein levels adversely affects the spermatogenesis and results in cellular depletion.