Cadmium induced oxidative damage and apoptosis in the hepatopancreas of Meretrix meretrix.

Even trace amounts of cadmium (Cd), a non-essential metal, are known to be toxic to aquatic organisms. Here we investigated the relationship between cadmium ion (Cd(2+)) exposure and oxidative damage and apoptosis in the hepatopancreas of the clam Meretrix meretrix. Clams were exposed to different concentrations of Cd(2+) (0, 1.5, 3, 6 and 12 mg L(-1)) for 5 days. We monitored both antioxidant enzyme activity, including that of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx), and levels of malondialdehyde (MDA), glutathione (GSH) and glutathione disulfide (GSSG). Apoptosis of hepatopancreatic cells was detected by DNA laddering and AO/EB double fluorescent staining. The results show that the rate of apoptotis, MDA levels, and caspase-3 activity, increased with Cd(2+) concentration, whereas GPx activity and the ratio of GSH/GSSG, decreased. SOD and CAT enzyme activity first increased, then decreased, with increasing Cd(2+) concentration; peak activity of these enzymes was recorded in the 3 mg L(-1) Cd(2+)-treatment group. These results show that Cd-induced oxidative damage can both induce, and aggravate, apoptosis in the hepatopancreatic cells of clams, even at Cd(2+) concentrations far below the semi-lethal dose for adult clams. The observed changes in caspase-3 activity enhanced significantly at lower Cd(2+) concentrations, indicating that caspase-3 is a suitable biomarker for heavy metal pollution, especially cadmium pollution, in marine organisms.