Cellular responses of oysters, Crassostrea virginica, to metal-contaminated sediments

Elevation of metal concentrations in coastal environments associated with anthropogenic enrichment pose a significant threat to estuarine organisms. The purpose of this study was to evaluate the relationships between cellular responses that may be potentially valuable as indicators of chronic stress and metal-contaminated sediments. For these studies, hatchery-reared juvenile oysters were deployed in situ at 15 sites for approximately 1 month around Charleston Harbor, SC. The effects on lysosomal destabilization and glutathione concentrations were determined; and the relationships between the cellular responses and sediment metal concentrations were described. Both single metal and multiple metal parameters (based on total metal concentrations, aluminum normalizations, and summed sediment quality guidelines) were considered. Generally, significant correlations were observed for individual metal analytes and multiple metal parameters. Since many of the individual metal analytes covary, the responses may reflect overall contaminant loading rather than responses to individual metals. Methods for estimating overall contaminant loading based on multiple analytes provide a more realistic estimate of potential adverse effects.     

The effects of glutathione depletion on reproductive success in oysters, Crassostrea virginica.

Glutathione (GSH) is a ubiquitous tripeptide that functions as a very important modulator of cellular homeostasis, including detoxification of metals and oxyradicals. Therefore, depletion of GSH may predispose organisms to pollutant stress. Reproductively active oysters (Crassostrea virginica) were exposed to buthionine sulfoximine in the laboratory to deplete gonadal GSH. The effects of metal exposures (Cd and Cu) on fertilization and developmental assays were evaluated using gametes from control and GSH-depleted adults. Fertilization success was not affected by GSH status, i.e. the fertilization rates of gametes derived from GSH-depleted adults were the same or slightly higher. However, GSH depletion did increase the susceptibility of developing embryos to metal toxicity, i.e. adverse effects on embryonic development were observed at lower metal concentrations with gametes derived from GSH-depleted adults. These effects may be related to diminished removal of free radicals or increased availability of metals. Whereas sperm penetration of embryonic membranes and fertilization success may be facilitated by free radicals, the persistence of free radicals during subsequent developmental periods may adversely affect differentiation and normal development. GSH probably also plays an important role in scavenging toxic metals and reducing metal interactions with essential developmental processes. These results suggest that parental depletion of GSH may increase the susceptibility of embryos to metal toxicity.