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Nicotine-induced damages in testicular tissue of rats; evidences for bcl-2, p53 and caspase-3 expression
Maryam Mosadegh1, Shapour Hasanzadeh1, Mazdak Razi1
1Department of Comparative Histology and Embryology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
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-1, IP) nicotine-received and high dose (0.4 mg/kg BW-1, 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 (P<0.05) reduction at mRNA and protein levels of bcl-2. More analyses revealed a remarkable (P<0.05) enhancement in expression of p53 and caspase-3 in comparison to control-sham animals. Finally, nicotine resulted in a significant (P<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.
Insights
Nicotine exposure harms sperm production by lowering testosterone and bcl-2 levels, while increasing p53 and caspase-3, leading to cell depletion and impaired spermatogenesis.
Area of Science:
- Reproductive Biology
- Toxicology
- Molecular Biology
Background:
- Nicotine is a widely consumed substance with known adverse health effects.
- Its impact on male reproductive function, specifically spermatogenesis, requires further elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms underlying nicotine-induced damage to spermatogenesis.
- To assess the effects of nicotine on key regulatory proteins and hormones involved in sperm production.
Main Methods:
- Wistar rats were exposed to low and high doses of nicotine for 7 weeks.
- Gene and protein expression of bcl-2, p53, and caspase-3 were analyzed using RT-PCR and IHC.
- Serum levels of FSH, LH, and testosterone were measured.
- mRNA damage was assessed via fluorescent staining.
Main Results:
- Nicotine reduced tubular differentiation, spermiogenesis, and repopulation indices, causing cellular depletion.
- A significant decrease in bcl-2 (mRNA and protein) and testosterone levels was observed.
- Expression of p53 and caspase-3 (mRNA and protein) significantly increased.
- Elevated mRNA damage was noted in nicotine-exposed groups.
Conclusions:
- Nicotine adversely affects spermatogenesis by suppressing testosterone biosynthesis and downregulating bcl-2.
- Upregulation of p53 and caspase-3 contributes to nicotine-induced cellular depletion in the testes.
- These findings highlight nicotine's detrimental role in male fertility.
