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Association between a Polymorphism of Aminolevulinate Dehydrogenase (ALAD) Gene and Blood Lead Levels in Japanese Subjects

By Koichi Miyaki, Htay Lwin, Katsunori Masaki, Yixuan Song, Yoshimitsu Takahashi, Masaaki Muramatsu and Takeo Nakayama


This cross-sectional study investigated the relationship between the aminolevulinate dehydrogenase (ALAD) genotype and blood lead levels among 101 Japanese workers. Blood lead concentration measurement, biomarkers, and genotyping were performed. The minor allele frequency (MAF) for ALAD (ALAD2) was 0.08. Although the blood lead level in the subjects with heterozygous GC genotype was significantly higher than those with homozygous GG genotype, there were no significant differences for hemoglobin, hematocrit, serum and urinary ALA levels among genotypes. ALAD2 genotype was significantly associated with the blood lead concentration, even in the environmental lead exposed subjects. Further confirmation with a large sample size is needed

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    1. (2008). A study on the ALAD gene polymorphisms associated with lead exposure.
    2. (2000). Association between aminolevulinate degydrogenase genotype and blood lead levels in
    3. (2007). Association Between delta-Aminolevulinic Acid Dehydratase (ALAD) Polymorphism and Blood Lead Levels: A Meta-regression Analysis.
    4. (1994). Blood lead levels in the general population of Taiwan,
    5. (2004). Delta-aminolevulinic acid dehydratase (ALAD) polymorphism and susceptibility of workers exposed to inorganic lead and its effects on neurobehavioral functions. Neurotoxicology
    6. (2001). Delta-aminolevulinic acid dehydratase genotype and lead toxicity: a HuGE review.
    7. (1997). Delta-aminolevulinic acid dehydratase genotype modifies four hour urinary lead excretion after oral administration of dimercaptosuccinic acid.
    8. (2000). Genetic susceptibility to lead poisoning. Environ. Health Perspect
    9. (1994). Influence of common human [delta]-aminolevulinate dehydratase polymorphism on lead body burden. Environ. Health Prospect.
    10. (2003). Influence of delta-aminolevulinic acid dehydratase (ALAD) polymorphism on the frequency of sister chromatid exchange (SCE) and the number of high-frequency cells (HFCs) in lymphocytes from lead-exposed workers.
    11. (2009). Influence of the delta-aminolevulinic acid dehydratase (ALAD) polymorphism on biomarkers of lead exposure in Turkish storage battery
    12. (2007). Interpreting and Managing Blood Lead Levels <10 µg/dL in Children and Reducing Childhood Exposures to Lead: Recommendations of CDC's
    13. (1991). Knowledge of diagnosis and reproductive history among survivors of childhood plumbism.
    14. (2004). Lack of Association of delta-amimnolevulinic acid dehydratase genotype with cytogenetic damage in lead workers.
    15. (2007). Lead and δ-Aminolevulinic Acid Dehydratase Polymorphism: Where Does It Lead? A Meta-Analysis. Environ. Health Perspect.
    16. (1984). Lead poisoning in inherited -amimnolevulinic acid dehydrogenase deficiency.
    17. (1998). Lead poisoning, haem synthesis and 5-aminolaevulinic acid dehydratase.
    18. (1995). Lead-induced nephropathy: relationship between various biological exposure indices and early markers of nephrotoxicity.
    19. (1987). Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development.
    20. (1989). Mechanisms of lead and cadmium nephrotoxicity.
    21. (1987). Occupational exposure to lead and blood pressure: a study in 105 workers.
    22. (2000). Relationship between delta-aminolevulinic acid dehydratase genotypes and heme precursors in lead workers.
    23. (1991). The [Delta]-aminoleuvulinate dehydratase polymorphism: higher blood lead levels in lead workers and environmentally exposed children with the 1-2 and 2-2 isoenzymes.
    24. (1991). The health effects of low level exposure to lead.
    25. (1990). The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report.
    26. (2001). The molecular mechanism of lead inhibition of human porphobilinogen synthase.
    27. (1996). Unraveling the chronic toxicity of lead: an essential priority for environmental health. Environ. Health Perspect.
    28. (1998). Urinary 5-aminolevuinic acid (ALA) adjusted by creatinine a surrogate for plasma ALA.

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