Cadmium-induced Oxidative Stress in Meretrix Meretrix Gills Leads to Mitochondria-mediated Apoptosis

Abstract Cadmium (Cd) is one of the most important marine environmental pollutants that can cause oxidative damage and apoptosis in living organisms, and mitochondria are the key target cell organelles of Cd toxicity. In this study, we investigated the effect of Cd on the mitochondria of Meretrix meretrix gill cells and the underlying mechanism of mitochondria-mediated apoptosis following exposure to the metal. Exposure of the clams to 1.5, 3, 6 and 12 mg L−1 Cd2+ solutions led to swollen mitochondria compared with the untreated clams. The mitochondria also became vacuolated at the higher Cd2+ concentrations. Biochemical assays showed that monoamine oxidase (MAO) activity and mitochondrial membrane potential (Δψm) increased at 1.5 mg L−1 Cd2+, but decreased at higher Cd2+ concentrations, while the activities of malate dehydrogenase (MDH) and cytochrome oxidase (CCO) and the scavenging capacities of anti-superoxide anion (ASA) and anti-hydroxy radical (AHR) all decreased with increasing Cd2+ concentrations. Significant increases in the levels of MDA and H2O2 as well as in the activity levels of caspase-3, -8, and -9 were also observed in the Cd2+-treated clams. The results implied that Cd might induce apoptosis in M. meretrix via the mitochondrial caspase-dependent pathway.