The inhibition of δ-aminolevulinic acid dehydratase (ALAD) in the heme synthetic pathway results in increased protophoryphyrin (ZPP) and δ-aminolevulinic acid (ALA) and is responsible for some of toxicological effects of lead. This enzyme is coded b...
The inhibition of δ-aminolevulinic acid dehydratase (ALAD) in the heme synthetic pathway results in increased protophoryphyrin (ZPP) and δ-aminolevulinic acid (ALA) and is responsible for some of toxicological effects of lead. This enzyme is coded by the ALAD gene containing 2 co-dominant alleles. The polymorphisms of ALAD gene may be related to differential effects of lead on ZPP and ALA, ALAD genotype was measured in 975 Korean male lead workers, of whom 897 were homozygous for ALAD1 (ALAD 1-1 genotype) and 96 were heterozygous for ALAD2 (ALAD 1-2 genotype). Blood lead in subjects with ALAD1 was significantly higher than those with ALAD2 (p = 0.01). No difference between ALAD genotypes was found for age, exposure duration, ZPP, ALA, hemoglobin, hematocrit, body mass index, tobacco and alcohol use. After adjustment for possible confounders, ALA and ZPP became significantly elevated in ALAD1 subjects (p = 0.004 and 0.055, respectively). This result suggests that ALAD1 subjects may be more susceptible to the hematotoxicologic effects of lead than ALAD2 subjects.