ENVIRONMENTAL SCIENCE AND MANAGEMENT

ABSTRACT The aminolevulinic acid dehydratase (ALAD) is an enzyme in the heme biosynthetic pathway and is sensitive to the action of heavy metals. Lead, a toxic heavy metal with a long half-time in the body, inhibits ALAD activity by binding the enzyme’s sulphydril group and results in neurotoxic aminolevulinic acidaccumulation in the blood and urine. During pregnancy, the fetus is at high risk from maternal lead exposure since lead from the mother can easily cross the placenta. The aim of this study was to determine whether the maternal ALAD G177C single-nucleotide polymorphism is related to the lead levels in placental tissue. The study population comprised 97 blood samples taken from mothers for investigating ALAD polymorphism and their placentas for measuring lead levels. ALAD polymorphism was detected by standard polymerase chain reaction (PCR) – restriction fragment length polymorphism (RFLP) technique and an atomic absorption spectrometer (AAS) equipped with a graphite furnace and Zeeman background correction system was used for lead determination. A total of 90 mothers had homozygote typical (ALAD1-1) genotype, 6 mothers had heterozygote (ALAD1-2) genotype, and 1 mother had homozygote atypical (ALAD2-2) genotype for ALAD polymorphism. The median placental lead levels for ALAD1-1, ALAD1-2 and ALAD2-2 genotypes were 7.54 ppb, 11.78 ppb and 18.53 ppb, respectively. Statistically significant association was found between the maternal ALAD gene polymorphism and their placental lead levels (p < 0.05). This study suggests that mothers with ALAD1-1 genotypes are more advantageous in terms of having lower placental lead levels than those with ALAD1-2 and ALAD2-2 genotypes.