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The Effects of Lead Exposure on the Activities of δ-Aminolevulinic Acid Dehydratase (ALAD) with the Modification of the Relative Genotypes

Hsieh, Chia-Chen; Liu, Te-Yu; Chiu, Yu-Wen; Chuang, Hung-Yi

doi: 10.1097/01.ede.0000362370.35141.f1
Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25–29, 2009: Symposium Abstracts

Kaohsiung Medical University, Kaohsiung City, Taiwan.


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Background and Objective:

To investigate the effects of blood lead and other related factors on δ-aminolevulinic acid dehydratase (ALAD) activity in lead workers.

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In 121 lead workers and 117 reference subjects, the following data were collected from health examination: blood lead, BMI, glucose AC, and Hct. A questionnaire including demographic data, medical history, smoking and alcohol consumption was completed by each of subjects. ALAD activity was determined by the standardized method of the European Community. ALAD polymorphism genotyping was using a method of PCR-RFLP.

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In this study, 229 ALAD1-1 homozygotes (96.2%), 8 ALAD1-2 heterozygotes (3.8%) were identified, and none of ALAD2-2 homozygote was observed. Blood lead levels in lead workers and reference subjects were 19.5 μg/dL (SD = 14.7) and 2.9 μg/dL (SD = 1.9), respectively. Lead workers had significantly lower ALAD activity than reference subjects (42.6 ± 22.4 U/L vs. 64.3 ± 13.8 U/L, P < 0.001). According to the multiple regression results, the following independent variables were significant related to ALAD activity: ALAD activity in females was much lower (8.15 U/L) than males (P < 0.001); blood lead and glucose AC were inversely associated with ALAD activity (P < 0.001), but the effect of blood lead was profound. The regression coefficients of blood lead and glucose AC were 1.04 and 0.11, respectively. Individuals with alcohol consumption showed lower ALAD activity (P = 0.049). The possible threshold value of blood lead for ALAD activity was determined at around 10 μg/dL.

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ALAD activity was inhibited by lead sensitively and stoichiometrically, thus ALAD activity may be adopted as a reliable biomarker of lead toxicity in humans.

© 2009 Lippincott Williams & Wilkins, Inc.