Abstract

Background: Cadmium is a serious environmental and occupational contaminant that may represent a serious health hazard to humans and other animals. Since cadmium cannot be degraded, the risk of environmental exposure is constantly increasing because of accumulation via the food chain. Exposure to cadmium at the cellular level can produce tissue injury and damage various organs, but the underlying mechanism is enigmatic. Methods: In order to investigate its toxicity on lipid profile and malondialdehyde concentration, thirty-two rats were exposed to 100, 200 and 300 ppm cadmium in their drinking water for six weeks while the control group received distilled water for the same period. Results: At all the concentrations, cadmium produced a significant (p<0.05) dosedependent hypocholesterolemia, hypotriglyceridemia and hypophospholipidemia in the plasma and erythrocyte respectively. Exposure to cadmium resulted in increased hepatic triacylglycerol concentration, whereas brain triacylglycerol concentrations were reduced. While cadmium induced brain phospholipidosis, a reduction in liver phospholipid concentration was observed. There was a significant (p<0.05) dose-dependent increase in the plasma, erythrocyte, brain and liver malondialdehyde concentrations corresponding to 56, 89, and 69 % at high dose of 300 ppm respectively compared to control. While positive associations were observed between plasma, liver, brain, erythrocyte malondialdehyde and organ triacylglycerol and phospholipid, negative associations were observed with liver phospholipid.

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