Attenuation of quinine-induced testicular toxicity by ascorbic acid in rat: a stereological approach

Quinine (QU), an alkaloid derived from the cinchona bark is presently the mainstay of treatment for severe malaria and nocturnal leg cramps. We have recently demonstrated that QU is toxic to testicular gonocytes and interstitial endocrinocytes. This present study sought to determine whether co-administration of ascorbic acid (AA) with QU will modify the deleterious effects of QU on the testes of Sprague-Dawley rats. 50 male Sprague-Dawley rats weighing 160-180g were used for the experiments. The animals were randomly divided into 5 groups of 10 rats each and were variously administered QU for 7 days, QU for 8 weeks, QU plus AA for 7 days, QU plus AA for 8 weeks and distilled water. They were all sacrificed on the 56th day. Histological slides of the testes were prepared and morphometric parameters that included diameter and cross-sectional area of the seminiferous tubules, number of profiles of seminiferous tubules per unit area of testis and numerical density of the seminiferous tubules, volume density and absolute volume of testicular components were determined using a systematic random scheme. Our results showed that the cytoarchitecture of seminiferous tubules of rats treated with QU only was grossly distorted, while that of rats that had both QU and AA was not significantly different from that of the controls. The testicular volume; diameter and cross-sectional area of seminiferous tubules; and the relative and absolute volume of seminiferous epithelium of QU-treated rats were significantly (P < 0.05) reduced, while those of QU plus AA-treated Ones were not significantly different from those of the controls. In contrast, the numerical density of the tubules were significantly (P < 0.05) increased in rats administered QU only, while it was not significantly different in the QU plus AA-treated and control rats. We conclude that co-administration of AA with QU could play an important role in the modulation of QU-induced testicular damage.