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As the δ-aminolevulinic acid dehydratase ( ALAD ) G177C polymorphism affects the toxicokinetics of lead in the body, and the corresponding exposure to lead may increase the risk of adult brain tumors, we hypothesize that there is a possible association of the ALAD G177C genotype and the risk of brain tumors in human. Therefore, the aim of the present study was to clarify the role of the ALAD enzyme gene polymorphism at position G177C in the pathogenesis of brain tumors and its correlation to lead exposure. The ALAD gene polymorphism at position G177C was genotyped using the polymerase chain reaction with restriction fragment length polymorphism method and measured the blood lead level by atomic absorption in 81 brain tumor patients and compared the results with 81 controls. The frequency of the GC genotype ( ALAD1-2 ) was significantly increased in primary brain tumor patients compared to the control group. The genotype frequency of ALAD2 (ALAD1-2 and ALAD2-2 ) was significantly higher in the meningioma patients but was not significant in glioma patients. There was no significant difference in the number of patients and blood lead level when compared with the control. There was a significant increase when compared to ALAD1 regarding a mean value of the lead level. The genotyping of the ALAD G177C polymorphism in the present study revealed a significant association between ALAD2 and brain tumors. The ALAD G177C polymorphism may modify the lead kinetics in the blood, is associated with higher blood lead burden and may provide a biomarker of neurotoxic risk.

Association between δ-aminolevulinate dehydratase G177C polymorphism and blood lead levels in brain tumor patients