Previous human and experimental studies have demonstrated that lead ex
posure may modify the metabolism of lipids. Several studies have indic
ated that exposure to lead produces an increase in lipid peroxidation
and inhibits blood superoxide dismutase activity. Recently, lipid pero
xides have been shown to impair tissue membranes and to be a risk fact
or 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. Exp
eriments 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 wi
th sodium acetate equimolar to the acetate in the lead acetate solutio
n. One day after the feeding was over, venous blood samples, under eth
er anesthesia, were collected. The animals were killed by exsanguinati
on and the liver was excised for determination of the metal (lead, cop
per, and zinc) content. A segment of the abdominal aorta was excised f
or histological examination. In venous blood the following were estima
ted: triglycerides, total cholesterol, high-density lipoprotein (HDL)-
cholesterol fraction, serum lipid peroxides, and blood superoxide dism
utase activity. Metal content (lead, copper, and zinc) in blood and li
ver was determined by means of atomic absorption spectrophotometry. In
rats poisoned with small doses of lead, decreases in the plasma chole
sterol level and the HDL-cholesterol fraction were observed. In parall
el with the decrease in the cholesterol concentration, lead increases
the serum triglyceride level, this increase being dependent upon lead
levels in blood. In our studies a significant influence of lead on ser
um lipid peroxide level or blood superoxide dismutase activity was not
found. In the histological examination, atrophy of the elastic fibers
in the aorta was observed. The possible significance of the inhibitor
y effect of lead on lipoprotein lipase activity is discussed.