The aim of the present study was to investigate whether curcumin (CUR) can ameliorate cadmium-induced reproductive toxicity and its mechanism. A total of 48 male mice were equally divided into 4 groups: control, CdCl2 (2 mg/kg, intraperitoneally inject) curcumin (50 mg/kg, intraperitoneally inject), co-treatment with curcumin (50 mg/kg), and CdCl2 (2 mg/kg) for 10 days. The results demonstrated that CdCl2 reduces sperm motility, decreases the sperm density and serum testosterone content, and significantly improves the rate of sperm deformity. CdCl2 increased the level of testicular total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px) activity, and glutathione (GSH), and CdCl2 declined the level of malondialdehyde (MDA). However, the semen quality of the mice in the curcumin intervention group was improved. Moreover, the testosterone content and antioxidant capacity were increased. In the Cd group mice, the expression of testicular Nrf2, as well as the mRNA and protein expressions of the downstream target molecules, glutathione peroxidase (GSH-Px), and γ-glutamylcysteine synthetase (γ-GCS) of Nrf2 declined, while the above genetic expressions elevated significantly in the curcumin intervention group. Our results suggested that curcumin could protect against Cd-induced testicular injury via activating the Nrf2/ARE signaling pathway.
Keywords: Cadmium; Curcumin; Mice; Nrf2/ARE pathway; Oxidative damage; Testes.