Mitochondrial pathway of apoptosis in the hepatopancreas of the freshwater crab Sinopotamon yangtsekiense exposed to cadmium

Cadmium (Cd) is one of the most common toxic metals in water. To investigate the mechanism of Cd-induced apoptosis in the hepatopancreas, freshwater crabs Sinopotamon yangtsekiense were exposed to 0, 3.56, 7.12, 14.25, 28.49 and 56.98 mg/L Cd for 48 h. After a 48 h exposure, apoptosis and necroptosis were apparent in the group exposed to 28.49 mg/L Cd and only one case of necrosis was observed in the highest concentration of Cd. Electronic microscopy revealed chromatin condensation under nuclear membrane and mitochondrial membrane rupture in 14.25 and 28.49 mg/L Cd treatment groups. Brown colored apoptotic cells were detected with the TUNEL test in all Cd-treatment groups. The AI in 56.98 mg/L group was 1.4-fold greater than that in crabs exposed to 14.25 mg/L Cd. Caspase-9, caspase-3, SDH and Ca2+-ATPase activities increased with increasing Cd concentration. However, the activities of caspase-8 and LDH did not change significantly compared with control group. These results implied that Cd induced apoptosis in the hepatopancreas occurs through a mitochondrial pathway.