Cadmium (Cd) has been widely used in industry and can accumulate in the water, soil, and food. Meretrix meretrix is one of the marine shellfishes cultivated for economic purpose in China. The increasing Cd levels in coastal marine water could adversely affect the economic benefits of shellfish cultivation. In the present study, M. meretrix were exposed to different Cd2+ concentrations (0, 1.5, 3, 6, and 12 mg L-1) for 5 d to evaluate the effects of Cd on spermatogenic cell. The Cd accumulation, survival rate and the indices of oxidative stress and apoptosis were determined in the spermatogenic cells of M. meretrix. The expression levels of p53 and metallothionein (MT) mRNA were also measured in the spermatogenic cells. Cd accumulation and the mortality rate of spermatogenic cells were found to increase in a dose-response manner with Cd2+ concentrations. Histopathology changes, especially the damage of membranous structure, were more severe as the Cd2+ levels in the testis became higher. The indexes of oxidative stress, including reactive oxygen species, malondialdehyde, protein carbonyl derivates and DNA-protein crosslinks all increased after exposure to Cd2+. However, the total antioxidant capacity gradually decreased with the increasing Cd2+ concentration. In addition, exposure to Cd2+ increased the apoptotic rate and caspase-3 and 9 activities but decreased the level of mitochondrial membrane potential and cytochrome C oxidase in the spermatogenic cells. MT mRNA expression increased in lower Cd2+ concentration treated groups whereas decreased in higher groups, while the p53 mRNA expression increased in a dose-response manner with Cd2+ and was positively correlated with the oxidative damage indices. These results indicated that Cd2+ caused oxidative stress and p53 induced apoptosis in the spermatogenic cells, and thus decreased the survival rate of sperm cells. This finding highlights that Cd can reduce the reproductive capacity of M. meretrix, thus threatening to wild shellfish populations and reducing the efficiency of shellfish farming.

Cadmium (Cd), one of the most toxic metals found in inshore sediments of China, is a persistent environmental contaminant capable of exerting irreversible toxic effects on aquatic organisms and their associated ecosystems. Although Cd is known to be toxic to marine animals, the underlying mechanism of this toxicity is not clear. In this study, Meretrix meretrix, a commercially and ecologically important species of clam, was exposed to different concentrations of cadmium chloride (0, 1.5, 3, 6, and 12 mg L^–1) for 5 days, and the levels of Cd accumulation, antioxidant enzyme activity, and expression of metallothionein (MT) in the hepatopancreas, gill, foot, and mantle were evaluated. The results revealed a sharp increase in Cd accumulation in the tissues in response to increased Cd²⁺ concentrations in the water, and significant differences in Cd accumulation were observed among the different tissues. Increased Cd²⁺ level in the tissues also led to a significant increase in malondialdehyde content, caused by increased lipid peroxidation. The activities of superoxide dismutase and catalase also increased, peaking at different Cd²⁺ concentrations, depending on the tissue. Glutathione peroxidase (GPx) activity in the gill and mantle initially increased but then decreased with increasing external Cd²⁺ concentration. In the hepatopancreas and foot, GPx activity was inhibited by Cd²⁺, even at low concentrations. Furthermore, Cd²⁺ also stimulated the expression of MT in all four tissues. However, the levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) in the gill and mantle, as well as the GSH/GSSG ratios in all four tissues, decreased with increasing external Cd²⁺ concentrations. Taken together, the results suggested that in M. meretrix, response to the toxic effect of Cd²⁺ might occur through a combination of mechanisms, which involve both enhanced antioxidant enzyme activities and the ability to bind and sequester Cd²⁺ via cysteine-rich molecules such as GSH and MT, both of which would eventually lead to the reduction of heavy metal-induced oxidative stress.