Exposure to waterborne cadmium induce disorder of lipid metabolism, antioxidant system and autophagy in the muscle of crayfish Procambarus clarkii

Cadmium (Cd) is a non-essential toxic metal in the body, which can cause harmful effects on the aquatic environment and aquatic organisms. In this study, the effects of acute Cd exposure on lipid metabolism disorder, oxidative stress and autophagy in abdominal muscles of Procambarus clarkii were investigated, as well the underlying molecular mechanisms were explored. P. clarkii were exposed to 0 (control), 1 and 5 mg Cd/l, respectively, for 5 days. We found that TG content, fas, hsl, and cpt1 gene expression levels, as well as the Srebp1 protein content in abdominal muscle decreased with the Cd concentrations increased, indicating that acute Cd exposure induced disorder of lipid metabolism in the abdominal muscle of P. clarkii. Further studies showed that acute Cd exposure provoked oxidative stress in the abdominal muscle of P. clarkii by increasing the accumulation of malondialdehyde (MDA) in the abdominal muscle. The oxidative stress of abdominal muscle induced by acute Cd exposure may be due to the reduction of catalases (CAT) and glutathione peroxidase (GPX) enzyme activities and Nrf2 protein content in the nucleus. The expression levels of autophagy-related genes (beclin1, atg101, atg13, atg3, atg4b, atg5, atg7, lc3a, lc3c atg9a) were also affected by acute Cd exposure, suggesting that acute Cd exposure also affected autophagy activity in abdominal muscle of P. clarkii. Our research indicates that waterborne acute Cd exposure can induce lipid metabolism disorder, and oxidative stress, and inhibit the expression of genes that trigger autophagy in the abdominal muscle of P. clarkii. These results may be useful for understanding the mechanism of Cd muscular toxicity in crustaceans.