This study aimed to investigate the effect of naringenin (Nar) on cadmium (Cd)-induced testicular toxicity. Twenty-four male Sprague-Dawley (SD) rats aged 5 weeks were used. Rats were administered with 0.9% NaCl (control group), CdCl2 (2 mg/kg b.w. intraperitoneally), Nar (50 mg/kg b.w, orally), and CdCl2 + Nar (2 mg/kg b.w intraperitoneally and 50 mg/kg b.w. orally, respectively) for 4 weeks. Results showed that body weight, relative testis weights, and sperm quality decreased in the Cd-treated group, and Cd accumulated in serum and testes. Pathological examination showed that Cd can cause testicular damage. Cd decreased the serum concentrations of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone. It also decreased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Moreover, exposure to Cd resulted in decreased content of reduced glutathione (GSH) and total antioxidant capacity (T-AOC) concentrations, as well as increased malondialdehyde (MDA) and hydrogen peroxide (H2O2) contents. Cd also provoked testis autophagy by upregulating the expression of the autophagy-related proteins P62 and LC3 II. However, the combined administration of Nar and Cd significantly attenuated the Cd-induced negative effects by increasing the body weight, relative testis weights, and sperm quality and by decreasing testicular damage. Simultaneous supplementation of Nar and Cd markedly restored the decreased levels of GnRH, FSH, LH, testosterone, GSH, and T-AOC and the activities of SOD, CAT, and GPx caused by Cd treatment. Nar further suppressed MDA and H2O2 production and protected the testes from Cd-induced autophagy by downregulating P62 and LC3 II expression. Therefore, Nar protected the testes from Cd-induced toxicity.