This study assessed the effect of quercetin (QE) on cadmium chloride (CdCl₂) − induced testicular toxicity, as well as the effect of withdrawal of CdCl₂ treatment on same. Thirty male Wistar rats aged 10 weeks old and weighing 270–300g were assigned into 5 groups and used for this study. Rats in groups 1–4 were administered vehicle, CdCl₂ (5mg/kg bwt), CdCl₂+QE (5mg/kg bwt and 20mg/kg bwt, respectively) or QE (20mg/kg bwt) orally for 4 weeks. Group 5 rats received CdCl₂, 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 CdCl₂ did not appreciably reverse toxicity. We conclude that QE better protected the testis from CdCl₂ toxicity than withdrawal of CdCl₂ administration.