Nicotine-induced damages in testicular tissue of rats; evidences for bcl-2, p53 and caspase-3 expression | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 14، دوره 20، شماره 2، 2017، صفحه 199-208 اصل مقاله (1.58 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2017.8249 | ||
| نویسندگان | ||
| Maryam Mosadegh؛ Shapour Hasanzadeh* ؛ Mazdak Razi | ||
| Department of Comparative Histology & Embryology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran | ||
| چکیده | ||
| Objective(s): 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. | ||
| کلیدواژهها | ||
| Apoptosis؛ Bcl-2؛ Caspase-3؛ Nicotine؛ P53؛ Testis؛ Testosterone | ||
| مراجع | ||
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