Nonsynergic Effect of Ethanol and Lead on Heme Metabolism in Rats

The heme biosynthetic pathway is a metabolic target of alcohol and lead poisoning. To analyze the interdependence of both xenobiotics on porphyrin metabolism, male Wistar rats (n=47) were divided into four groups and were fed Lieber–DeCarli semiliquid control or alcoholic diets containing or not containing lead acetate (160 mg/liter) for 8 weeks. After this period, hematocrit values and porphyrin concentration in liver and urine were similar in all groups, indicating that the goal of inducing only mild chronic intoxication was achieved. Compared with the control group, rats poisoned only with lead exhibited high levels of this metal in blood and liver, increased erythrocytic protoporphyrin, and hypoactivity of aminolevulinate dehydrase (ALA-D) in both blood and liver. Rats intoxicated only with alcohol exhibited mild hypoactivity of both hepatic and erythrocytic ALA-D, although such decreased enzymatic values did not achieve statistical significance. Rats receiving ethanol and lead simultaneously demonstrated abnormalities in heme biosynthesis similar to those in rats exposed to lead, although zinc hepatic levels decreased significantly only in animals exposed to both xenobiotics. Hepatic GSH and urinary ALA and porphyrin levels were maintained in a similar range in all groups.