Selenium mitigated cadmium-induced ovarian retardation in female Procambarus clarkii by regulating vitellogenin synthesis and transfer in the hepatopancreas.

Cadmium (Cd) is prevalent in aquatic ecosystems and accumulates in various tissues of aquatic organisms, leading to severe biological toxicity. Selenium (Se) is recognized for mitigating heavy metal toxicity, though its protective effects against Cd in aquatic crustaceans remain underexplored. This study, therefore, assessed the effects of dietary Cd (15 mg/kg) exposure and Se (6 mg/kg) supplementation on the hepatopancreas and ovaries of female crayfish to uncover the mechanisms of Cd toxicity and the protective role of Se. The results showed that Cd accumulation in the hepatopancreas caused a reduced hepatopancreas index (HPI), decreased protein content, histopathological damage, and oxidative stress, while Se supplementation reduced Cd levels, mitigated damage, and restored tissue integrity and antioxidant defenses. Transcriptomic analysis further revealed significant alterations in gene expression related to detoxification, lipid metabolism, and energy production in response to Cd exposure, which were partially or fully restored by Se supplementation. Additionally, Se alleviated Cd-induced inhibition of ovarian development, as evidenced by improved ovary index, enhanced oocyte development, and normalization of essential trace element levels. Mechanistically, Se restored the Cd-disrupted vitellogenin (Vtg) synthesis in the hepatopancreas via regulating the mRNA expression of hsp70 and genes related to the molt-inhibiting hormone (MIH) (mih, rxr, and ecr). Overall, these findings indicate that Se supplementation mitigated Cd-induced hepatopancreatic dysfunction, restored Vtg synthesis, and consequently counteracted the inhibition of ovarian development in adult female crayfish.