Abstract
Cadmium is a wide-spread environmental pollutant, redox-active metal that mainly accumulates in the liver and kidney, bones, pancreas and adrenals, rarely in the brain. The mechanisms of Cd toxicity are poorly understood, although some studies indicate that cellular damage results from an increase in production of reactive oxygen species and inhibition of antioxidant enzymes. We tested the hypothesis that acute Cd exposure would lead to increased oxidative damage in various brain regions (prefrontal cortex, hippocampus, nc.caudatus). Adult male rats were treated either with a single dose of 50 ppm of CdCl2 (LD50), or a single dose of 100 ppm CdCl2 (LD50), against control group not exposed to Cd. The enzymatic activity of total and mitochondrial SOD, as well as GR was significantly and dose depending decreased, but MDA content has shown only a moderate increase. Results demonstrated the harmful effects of acute Cd exposure, in the nervous tissue, through mechanisms of oxidative damage.
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