Cadmium (Cd), a highly toxic heavy metal, adversely affects human and animal health. Quercetin (Que) is a kind of flavonoid that can protect many tissues from the toxic effect of heavy metals. Although many studies have explored the adverse effects of cadmium on rats and other animals, the mechanism of Cd-induced testicular autophagy and the antagonistic effect of Que on cadmium remain unclear. In this study, Sprague-Dawley rats were treated with Cd, Que or Cd, and Que supplements to explore the mechanisms of Que-alleviated testis injury caused by Cd exposure. The rat body weight and relative testicular weight were measured. Morphological changes in testes and indices of oxidative stress were also examined. The expression levels of autophagy-related genes were detected as well. Results showed that Cd decreased the rat body weight and relative testicular weight and induced pathological changes in testes. Conversely, Que alleviated these changes. We also found that Cd increased the malondialdehyde content and decreased the contents of total superoxide dismutase, glutathione peroxidase, catalase, and glutathione. Moreover, the protein expression levels of P62 and LC3-II increased under Cd exposure conditions. Conversely, Que obviously alleviated these toxic activities induced by Cd. Overall, this study showed that Cd accumulated in rat testes, leading to oxidative stress and autophagy. Que can reduce cadmium toxicity by reducing oxidative stress and inhibiting autophagy. The specific mechanism of Que antagonizing Cd toxicity can provide new insights into countering cadmium toxicity.
Keywords: Autophagy; Cadmium; LC3B; Oxidative stress; P62; Quercetin; Rat; Testes.