Cadmium chloride–induced testicular toxicity in male wistar rats; prophylactic effect of quercetin, and assessment of testicular recovery following cadmium chloride withdrawal

摘要

Highlights ? Cadmium accumulates in the testis, causing oxidative stress and germ cell apoptosis. ? Cadmium suppresses spermatogenesis with poor reversal after withdrawal of exposure. ? Quercetin ameliorates CdCl 2 –induced testicular damage via its anti-oxidant and anti-apoptotic actions. Abstract This study assessed the effect of quercetin (QE) on cadmium chloride (CdCl 2 ) ? induced testicular toxicity, as well as the effect of withdrawal of CdCl 2 treatment on same. Thirty male Wistar rats aged 10 weeks old and weighing 270–300 g were assigned into 5 groups and used for this study. Rats in groups 1–4 were administered vehicle, CdCl 2 (5 mg/kg bwt), CdCl 2 + QE (5 mg/kg bwt and 20 mg/kg bwt, respectively) or QE (20 mg/kg bwt) orally for 4 weeks. Group 5 rats received CdCl 2 , with 4 weeks recovery period. Results showed that cadmium accumulated in serum, testis and epididymis, decreased body weight, testicular and epididymal weights, sperm count, motility and viability. Cadmium decreased serum concentrations of reproductive hormones, but increased testicular glucose, lactate and lactate dehydrogenase activity. Cadmium decreased testicular enzymatic (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymatic (glutathione, vitamins C and E) antioxidants, and increased malondialdehyde and hydrogen peroxide. Cadmium down-regulated Bcl-2 protein, up-regulated Bax protein, increased Bax/Bcl-2 ratio and cleaved caspase-3 activity. Histopathology of the testis showed decreased Johnsen’s score and Leydig cell count. These negative effects were attenuated by QE administration, while withdrawal of CdCl 2 did not appreciably reverse toxicity. We conclude that QE better protected the testis from CdCl 2 toxicity than withdrawal of CdCl 2 administration. ]]>