期刊
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH
卷 55, 期 1, 页码 -出版社
ASSOC BRAS DIVULG CIENTIFICA
DOI: 10.1590/1414-431X2021e11614
关键词
Chemotherapeutic drugs; Testes; Melatonin; Histology; Immunohistochemistry; Ultrastructure
资金
- Deanship of Scientific Research at King Khalid University, Abha, Kingdom of Saudi Arabia [R.G.P.2/122/42]
The aim of this study was to investigate the toxic effects of taxol on rat testes and the protective impact of melatonin against these effects. The results showed that melatonin could alleviate the damage caused by taxol on the testes by modulating apoptotic factors.
The aim of the present investigation was to study the toxic influences of taxol (TXL) on the testes of rats and the protective impact of melatonin (MLT) against such effects. Rats were classified into control, sham, TXL, MLT, and MLT+ TXL-treated groups. Histological and ultrastructural changes were observed in testicular tissues of TXL-intoxicated rats including thickening of tunica albuginea and degenerative alterations in spermatogenic, Sertoli, and Leydig cells. A significant increase (P <= 0.05) was found in the thickness of tunica albuginea and numbers of tubules without sperm, apoptotic germinal epithelia, and apoptotic Leydig cells, whereas the diameter of tubules and height of germinal epithelia displayed a significant decrease (P <= 0.05) compared with the control, sham, and MLT-treated groups. Immunohistochemically, a marked decrease (P <= 0.05) in Bcl-2 immunoreactivity and significant elevation (P <= 0.05) in P53 and caspase-3 immunoreactivities were recorded. Co-treatment of MLT and TXL modulated such histological, histomorphometrical, and ultrastructural changes induced by TXL. Also, MLT had a protective effect against testicular apoptosis induced by TXL, as shown by the elevated expression of Bcl-2 and decreased expression of P53 and caspase-3. In conclusion, the current investigation proved that MLT had a protective role against TXL-induced testicular cytotoxicity, which may be a result of inhibition of testicular apoptosis.
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