Effect of Vitamin E on δ-Aminolevulinic Acid Dehydratase Activity in Weanling Rabbits with Chronic Plumbism

Abstract

Lead inhibits several enzymes in the heme synthesis pathway with S-aminolevulinicacid dehydratase (ALAD) being the most sensitive. Vitamin E has a stimulatory effect on heme synthesis, apparently through its action on ALAD and on 5-aminolevulinic acid synthetase (ALAS). To study the possible effects of vitamin E in alleviating lead toxicity, rabbits were fed for 12 weeks a basal ration plus lead, either 25 mgAg body weight/day, or no lead, and one of four supplementary dl-a-to- copheryl acetate intakes equivalent to either 0, 1, 3, or 9 mg of itt-a-tocopherol/kg body weight/day. Equalized feeding of the basal ration was employed. Body weight was unaffected. In the lead-fed groups, plasma tocopherol was higher, whole blood lead concentration twice and liver lead four times greater. The concentration of liver lead increased 8 jug/100 g of fresh liver for each 10% increase in dietary tocopherol for those rabbits receiving vitamin E and lead. ALAD activity was depressed by lead; however, its activity was unaltered by vitamin E. Hematocrit levels were found to be lower in the plus-lead groups, incidence of basophilic stippling of erythrocytes greater, and urinary 5-aminolevulinicacid (UALA) and porphobilinogen greater. In rabbits fed lead, UALAconcentration was increased by 1.02 mg ALA/100 ml for each 10% increase in vitamin E. Based upon these findings, it is suggested that vitamin E may have had an effect on the enzyme ALAS, rather than on ALAD. J. Nutr. 104: 1637-1645,