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Abstract
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.