Abstract
Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipids. Several studies have indicated that exposure to lead produces an increase in lipid peroxidation and inhibits blood superoxide dismutase activity. Recently, lipid peroxides have been shown to impair tissue membranes and to be a risk factor for vascular diseases. The aim of the present investigation was to evaluate the impact of subclinical lead poisoning on rat lipids in the context of atherosclerosis. The degree of poisoning was analogous to that in populations exposed to lead in a contaminated environment. Experiments were performed on male Buffalo rats with body weights of 150-200 g. The experimental animals received lead acetate intragastrically in doses of 35 mg lead/kg body wt. (Pb/kg) once weekly or 70 mg Pb/kg twice weekly for 7 weeks. Control rats were fed in the same manner with sodium acetate equimolar to the acetate in the lead acetate solution. One day after the feeding was over, venous blood samples, under ether anesthesia, were collected. The animals were killed by exsanguination and the liver was excised for determination of the metal (lead, copper, and zinc) content. A segment of the abdominal aorta was excised for histological examination. In venous blood the following were estimated: triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol fraction, serum lipid peroxides, and blood superoxide dismutase activity. Metal content (lead, copper, and zinc) in blood and liver was determined by means of atomic absorption spectrophotometry. In rats poisoned with small doses of lead, decreases in the plasma cholesterol level and the HDL-cholesterol fraction were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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