Quercetin protects against testicular toxicity induced by chronic administration of therapeutic dose of quinine sulfate in rats

Abstract

Quinine, a rapidly acting blood schizonticide with a long history of use for the treatment of malaria, is gradually been implicated in reproductive toxicity. In this study, testicular and spermatotoxic effects of quinine sulfate (QS) following treatment with an oral dose of 10 mg/kg/day (normal therapeutic dose) for 8 weeks was investigated in male albino rats. Toxicity was evaluated by assessing antioxidant defense capacity and markers of oxidative stress and testicular dysfunction in the testes and epididymal sperm. The possible ameliorative effect of quercetin (QC), when co-administered with QS, was also assessed. Administration of QS induced oxidative stress in rats. The activities of superoxide dismutase, catalase, and malondialdehyde (a marker of lipid peroxidation) increased (p<0.05) both in the testes and epididymal sperm following QS treatment when compared with saline-treated (control) rats. Ascorbic acid levels were significantly reduced, with an insignificant decrease in glutathione and testosterone levels in the QS-treated rats, when compared with control. The spermiogram decreased with increase in total sperm abnormalities in QS-treated rats and was associated with histopathological changes. Our results revealed that QC significantly ameliorated QS-induced testicular toxicity and oxidative stress. The testicular toxicity of QS is in part due to impairment of testicular antioxidant defense, spermatogenesis and enhancement of lipid peroxidation. Also, the ability of QC to reverse the deleterious effects of QS on the testes and epididymis qualifies it as a potent chemo-protective agent against QS-induced reproductive toxicity.