Cell damage and apoptosis in the hepatopancreas of Eriocheir sinensis induced by cadmium

Cadmium (Cd) is one of the most common pollutants in the environment and it is known to cause a range of tissue damages and apoptosis in invertebrates. In this study, we investigated the effect of Cd on the hepatopancreas of the crab Eriocheir sinensis, a commercially and ecologically important species of crustacean. The crabs were first exposed to water containing different concentrations of Cd2+ (0, 0.63, 1.26, 2.52, 5.04 and 10.07 mg/L) for 6 days. Typical morphological characteristics and physiological changes of apoptosis were then observed using various methods, including AO/EB double fluorescence staining, transmission electron microscopy and DNA fragmentation analysis. The results showed that Cd2+ induced cell damage and apoptosis in a concentration-dependent manner. Transmission electron microscopy revealed the presence of cellular swelling and necrosis with reduced number of microvilli on the cell surface and damages to individual organelles. The mitochondria became swollen and vacuolated. The rough endoplasmic reticulum (Rer) was expanded, with membrane rupture and many different sizes of vesicles, suggesting the destruction of protein-synthesizing structures in the hepatopancreatic cells. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidases (GPx) initially increased and subsequently decreased with increasing Cd2+ concentrations. This was accompanied by increases in malondialdehyde (MDA) and H2O2 contents, which led to membrane lipid peroxidation. Crabs exposed to Cd2+ also displayed significant increases in caspase-3, -8, and -9 activities compared to control crabs. Cadmium induced the production and accumulation of ROS in the hepatopancreas, which resulted in oxidative damage and abnormal metabolism. Taken together, the results indicated that Cd2+ could induce oxidative damage as well caspase-dependent apoptosis in E. sinensis hepatopancreas.