δ-Aminolevulinic acid dehydratase activity, urinary δ-aminolevulinic acid concentration and zinc protoporphyrin level among people with low level of lead exposure

Wang, Qi; Zhao, Huan-hu; Chen, Jianwei; Qiaoling, Hao; Gu, Kangding; Zhu, Ye-xiang; Zhou, Yikai; Lin-xiang, YE

doi:10.1016/j.ijheh.2009.08.003

Cited by 22 publications

(10 citation statements)

References 30 publications

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“…Significant Our study also showed that children aged 0-12 years had a higher mean blood lead level ((107.52 ± 46.94 μg/L) than adolescents aged 13-17 (86.91 ± 40.45 μg/L). These results are in agreement with those found in the literature [39]. This was because young children spend a lot of time playing outside and a no significant difference was observed, the same as in a study conducted in Colombia [9].…”

Section: Discussionsupporting

confidence: 93%

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2019

J Toxicol Risk Assess

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Lead exists naturally in the earth's crust and it is widely used as a heavy metal. It is an environment toxicant that may deleteriously affect nervous, hematopoietic, skeletal, renal, endocrine and reproductive systems. So, exposure to lead in the environment continues to be a serious public health problem for all ages. Children are particularly susceptible to lead poisoning. They absorb more lead from their environment and their developing central nervous systems are vulnerable to the toxic. Fifty percent of children aged from 0 to 17-years-old presented blood lead levels above 100 μg/L and forty three percent of the same population presented blood lead levels above 50 μg/L. There was no correlation between urinary lead level and D-ALAU (urinary δ-aminolevulinic acid) with lead blood levels. But it was observed a small correlation between urinary lead and blood lead concentrations.

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Section: Discussionsupporting

confidence: 93%

“…Principal component analysis (PCA) showed that ALAU is not significantly associated with blood lead. This confirms the hypothesis that the ALAU assay is not a good biological indicator of lead exposure because hereditary tyrosinemia, liver diseases and stress, whatever the cause, can also increase ALAU [26,39].…”

Section: Discussionsupporting

confidence: 82%

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2019

J Toxicol Risk Assess

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“…Heme synthesis is significantly suppressed by lead through inhibition of three major enzymes involved in this pathway, including δ-aminolevulinic acid dehydratase (ALAD), aminolevulinic acid synthetase (ALAS), and ferrochelatase [25][26] while its effect on ALAD is more profound. In addition, lead is capable to induce oxidative damage to erythrocyte proteins and membrane at high concentrations which plays an important role in erythrocyte destruction.…”

Section: Discussionmentioning

confidence: 99%

Comparative Effect of Silymarin and D-Penicillamine on Lead Induced Hemotoxicity and Oxidative Stress in Rat

Jalali

Najafzadeh

Mousavi

2017

IJT

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“…Pb effects on heme synthesis are well documented [125, 126] and delta-ALA and ALAD levels in blood are considered the most reliable indicators of Pb intoxication [40, 127, 128], even at relatively low Pb blood concentrations [40]. Since inhibition of ALAD activity results in elevated delta-ALA levels in blood, consequential increase of urinary delta-ALA excretion is expected, and in fact, urinary delta-ALA has been used in clinical diagnosis of chronic occupational Pb intoxication [129]. However, urinary delta-ALA does not seem to be a sensitive indicator when Pb exposure is low [130].…”

Section: Biomarkers For Lead (Pb) Arsenic (As) and Manganese (Mn)mentioning

confidence: 99%

Lead, Arsenic, and Manganese Metal Mixture Exposures: Focus on Biomarkers of Effect

Andrade

Mateus

Batoréu

et al. 2015

Biol Trace Elem Res

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Summary The increasing exposure of human populations to excessive levels of metals continues to represent a matter of public health concern. Several biomarkers have been studied and proposed for the detection of adverse health effects induced by lead (Pb), arsenic (As) and manganese (Mn); however, these studies have relied on exposures to each single metal, which fails to replicate real-life exposure scenarios. These 3 metals are commonly detected in different environmental, occupational and food contexts and they share common neurotoxic effects, which are progressive and once clinically apparent may be irreversible. Thus, chronic exposure to low levels of a mixture of these metals represents an additive risk of toxicity. Building upon their shared mechanisms of toxicity, such as oxidative stress, interference with neurotransmitters and effects on hematopoietic system, we address putative biomarkers, which may be assist in assessing onset of neurological diseases associated with exposure to this metal mixture.

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δ-Aminolevulinic acid dehydratase activity, urinary δ-aminolevulinic acid concentration and zinc protoporphyrin level among people with low level of lead exposure

Cited by 22 publications

References 30 publications

Untitled

Untitled

Comparative Effect of Silymarin and D-Penicillamine on Lead Induced Hemotoxicity and Oxidative Stress in Rat

Lead, Arsenic, and Manganese Metal Mixture Exposures: Focus on Biomarkers of Effect

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