A representative gel of ALAD following a restriction fragment length digestion

Background: Rapid industrialization, urbanization, and population explosion in sub-Saharan Africa escalate environmental lead levels and subsequently blood lead levels in children. Its levels in one’s environment account for his/her blood lead levels. One’s susceptibility to lead toxicity is governed by his/her nutrition status, age and genetics. This study aimed at expounding susceptibility to lead toxicity by relating blood lead levels, delta-aminolevulinic acid dehydratase (ALAD) enzyme activity, and genetic variations of proteins that code for ALAD in urban children of Uganda. Methods: A total of 198 blood samples were spectrophotometrically analyzed for blood lead levels (BLL), hemoglobin (Hb) levels, and ALAD enzyme activity before DNA extraction, polymerase chain reaction, and restriction fragment length digestion for ALAD polymorphism.  Results: Up to 99.5% of the total samples analysed coded for ALAD1 allele compared to 0.05% that coded for ALAD2. There was a significant relationship between BLL, Hb status and ALAD enzyme activity in the three isozymes (ALAD1-1, ALAD1-2 and ALAD2-2) in strength of ALAD1-1 (r = 0.42, p-value = 0.02) ˂ALAD1-2 (r = 0.62, p-value = ˂0.001) ˂ ALAD2-2 (r = 0.67, p-value = ˂0.001). Conclusions: The majority of children in Uganda code for the ALAD1 allele, which is important for blood lead ions hoarding during lead toxicity. Hoarding of blood lead not only delays exposure effects but also accumulates its levels in deposit tissues and this poses adverse effects later in their lives. The data set was obtained from blood samples collected from children living in a Lead polluted urban setting, the DNA was extracted from all samples prior to a restriction fragment length digestion.