الفهرس | Only 14 pages are availabe for public view |
Abstract Drug-induced testicular toxicity is an extremely common condition and is responsible for a variety of pathological effects on the testes. Cisplatin (CIS), one of the most effective and potent anticancer drugs, is used in the treatment of a wide variety of both pediatric and adult malignancies. Despite the prevalent clinical applications of cisplatin, serious toxic side effects comprising reproductive toxicity confine its therapeutic efficacy. The present study was performed to elucidate some of the mechanisms involved in the testicular protective effects of captopril (Cap), telmisartan (Tel), carvedilol (Car), and L-carnitine (L-car) in experimentally cisplatin-induced testicular toxicity in rats. Male adult Sprague Dawley rats were divided into (i) normal untreated rats, (ii) 0.5 % carboxymethyle cellulose (CMC) (10 ml/kg/day, p.o, 15 days) treated rats, (iii) CIS (10 mg/kg; i.p.) treated rats to serve as testicular toxic control group, (iv) Cap (100 mg/kg/day, p.o, 15 days) treated rats, (v) Tel (10 mg/kg/day, p.o, 15 days) treated rats, (vi) Car (10 mg/kg/day, p.o, 15 days) treated rats,(vii) L-car (500 mg/kg/day, i.p, 15 days) treated rats, (viii) Cap+CIS treated rats, (ix) Tel+CIS treated rats, (x) Car+CIS treated rats, (xi) L-car+CIS treated rats. Cisplatin prominently decreased reproductive organs weights, sperm count, sperm motility, and increased sperm abnormalities, along with histopathological damage of testicular tissues |