Toxicity and bioaccumulation of the booster biocide copper pyrithione, copper 2-pyridinethiol-1-oxide, in gill tissues of Salvelinus fontinalis (brook trout).

This investigation studied the acute effects of copper pyrithione (CuPT) exposure on juvenile brook trout, Salvelinus fontinalis. Morphologic changes, copper bioaccumulation, and markers of oxidative stress in gill tissue were studied. Juvenile brook trout were treated with one of six experimental doses of CuPT (2-64 microg/L) for 2 hours. A seventh group served as a control population. Inductively coupled plasma atomic absorbance spectrophotometry (ICPAAS) analysis demonstrates significantly increased levels of copper in gill tissue (p < 0.001). Results from scanning electron microscopy and histological analysis demonstrate the formation of club-shaped lamella, edema, fusion of secondary lamella, loss of microridge structures and epithelial exfoliation. Transmission electron microscopy revealed altered morphology of chloride cells, including the swollen appearance of mitochondria with disruption of internal cristae and lipid membrane disruption. Thiobarbituric acid reactive substance (TBARS) assays demonstrated increased levels of lipid peroxidation products in gill tissue. Assays for the total antioxidant capacity of gill tissue revealed significantly lowered antioxidant levels. This data indicates that CuPT is potentially harmful to nontarget aquatic organisms at environmentally relevant doses.

Toxicity and bioaccumulation of the wood preservative copper dimethyldithiocarbamate in tissues of Long-Evans rats.

This study examined the toxicity and accumulation of copper in the livers and kidneys of Long-Evans rats after a subacute exposure to copper dimethyldithiocarbamate (CDCC) wood preservative. CDDC was recently introduced as an alternative to chromated copper arsenate (CCA) preserved wood. Female rats (220-270 g) were treated with 0, 25, 50, or 75 mg/kg CDDC by oral gavage for 3 wk. Light microscopy revealed that higher doses of CDDC induced diffuse necrosis and a loss of sinusoids in the livers of Long-Evans rats with vacuolization in the highest dose. Rats treated with 25 mg/kg CDDC displayed a thickening of the basement membrane of Bowman's capsule and the mesangium. Exposure to higher CDDC concentrations (50 and 75 mg/kg) showed moderate to marked expansion of the mesangial matrix and glomerular necrosis with an overall loss of glomerular structure seen in the highest dose. The concentration of copper was significantly increased in the tissues of animals exposed to CDDC in a dose-dependent manner. Western blot analysis revealed the induction of the stress protein Hsp70 and the formation of 4-hydroxy-2-nonenal (4HNE) adducts in liver and renal tissues, indicating peroxidative damage. CDDC was shown to be toxic to the livers and kidneys, at all doses used, and this toxicity is related to peroxidative insult.

The effects of the wood preservative copper dimethyldithiocarbamate in the hippocampus of maternal and newborn Long-Evans rats.

The potential toxic effects on human health and deleterious effects to the environment by copper dimethyldithiocarbamate (CDDC), an alternative wood preservative to chromated copper arsenate (CCA) have not been investigated. This study describes the neurotoxicity and accumulation of copper in the hippocampus of maternal and newborn Long-Evans rats following a subacute exposure to CDDC. Pregnant rats (220-270g) were treated daily with 0mg/kg, 25mg/kg, 50mg/kg, or 75mg/kg CDDC by oral gavage starting from day 6 of gestation and continuing to parturition. Following parturition, maternal and newborn rats were euthanized and brain tissues were removed, processed, and stored for analysis. Electron microscopy revealed demyelination and by-products of peroxidative damage in treated maternal hippocampi. Treated newborn hippocampi exhibited numerous degenerating mitochondria, membrane bound inclusion bodies, and vacuoles containing degraded structures. Graphite furnace atomic absorption spectrophotometry (GFAAS) demonstrated a significant increase in copper concentration in the tissues of treated animals as compared to controls. Western blot analysis revealed an induction of stress proteins HO-1 and Hsp70 and the formation of 4-hydroxy-2-nonenal (4HNE) adducts. CDDC was shown to be toxic to the brains, at all doses used and this toxicity is attributable to copper-induced lipid peroxidation.