ArticleNeurotoxicology and teratology
δ-Aminolevulinic acid dehydratase single nucleotide polymorphism 2 (ALAD2) and peptide transporter 2*2 haplotype (hPEPT2*2) differently influence neurobehavior in low-level lead exposed children.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of the δ-aminolevulinic acid dehydratase polymorphism rs1800435 on blood lead levels: a new systematic review and meta-analysis.Scientific reports · 2025Pooled it
- Effects of Blood Lead Levels <10 µg/dL in School-Age Children and Adolescents: A Scoping Review.Pediatrics · 2024Article
- Proton-Coupled Oligopeptide Transport (Slc15) in the Brain: Past and Future Research.Pharmaceutical research · 2023Review
- Pathogenesis of acute encephalopathy in acute hepatic porphyria.Journal of neurology · 2023Article
- Improving Equitability and Inclusion for Testing and Detection of Lead Poisoning in US Children.The Milbank quarterly · 2023Article
- An interdisciplinary team-based approach for significantly reducing lower-level lead poisoning in U.S. children.Toxicology reports · 2023Article
- Article
- Delta-Aminolevulinic Acid Dehydratase, Low Blood Lead Levels, Social Factors, and Intellectual Function in an Afro-Brazilian Children Community.Biological trace element research · 2022Article
- Kidney Involvement in Acute Hepatic Porphyrias: Pathophysiology and Diagnostic Implications.Diagnostics (Basel, Switzerland) · 2021Review
- Mechanisms of Neuronal Damage in Acute Hepatic Porphyrias.Diagnostics (Basel, Switzerland) · 2021Review
- Maternal Δ-aminolevulinic acid dehydratase 1-2 genotype enhances fetal lead exposure and increases the susceptibility to the development of cerebral palsy.Environmental science and pollution research international · 2020Article
- Recent advances in the epidemiology and genetics of acute intermittent porphyria.Intractable & rare diseases research · 2020Review
- Early chronic low-level lead exposure reduced C-C chemokine receptor 7 in hippocampal microglia.Toxicology letters · 2019Article
- Long-term consequences of early postnatal lead exposure on hippocampal synaptic activity in adult mice.Brain and behavior · 2019Article
- Genetic polymorphisms of GRIN2A and GRIN2B modify the neurobehavioral effects of low-level lead exposure in children.Environmental research · 2018Article
- A Variant of Peptide Transporter 2 Predicts the Severity of Porphyria-Associated Kidney Disease.Journal of the American Society of Nephrology : JASN · 2017Observational
- Influence of peptide transporter 2 (PEPT2) on the distribution of cefadroxil in mouse brain: A microdialysis study.Biochemical pharmacology · 2017Article
- Olfactory recognition memory is disrupted in young mice with chronic low-level lead exposure.Toxicology letters · 2015Article
- Relationship among maternal blood lead, ALAD gene polymorphism and neonatal neurobehavioral development.International journal of clinical and experimental pathology · 2015Article
- Potential frameworks to support evaluation of mechanistic data for developmental neurotoxicity outcomes: A symposium report.Neurotoxicology and teratologyArticle
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5 authors.
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Abstract
Delta-aminolevulinic acid dehydratase single nucleotide polymorphism 2 (ALAD2) and peptide transporter haplotype 2*2 (hPEPT2*2) through different pathways can increase brain levels of delta-aminolevulinic acid and are associated with higher blood lead burden in young children. Past child and adult findings regarding ALAD2 and neurobehavior have been inconsistent, and the possible association of hPEPT2*2 and neurobehavior has not yet been examined. Mean blood lead level (BLL), genotype, and neurobehavioral function (fine motor dexterity, working memory, visual attention and short-term memory) were assessed in 206 males and 215 females ages 5.1-11.8years. Ninety-six percent of children had BLLs<5.0μg/dl. After adjusting for covariates (sex, age and mother's level of education) and sibling exclusion (N=252), generalized linear mixed model analyses showed opposite effects for the ALAD2 and hPEPT2*2 genetic variants. Significant effects for ALAD2 were observed only as interactions with BLL and the results suggested that ALAD2 was neuroprotective. As BLL increased, ALAD2 was associated with enhanced visual attention and enhanced working memory (fewer commission errors). Independent of BLL, hPEPT2*2 predicted poorer motor dexterity and poorer working memory (more commission errors). BLL alone predicted poorer working memory from increased omission errors. The findings provided further substantiation that (independent of the genetic variants examined) lowest-level lead exposure disrupted early neurobehavioral function, and suggested that common genetic variants alter the neurotoxic potential of low-level lead. ALAD2 and hPEPT2*2 may be valuable markers of risk, and indicate novel mechanisms of lead-induced neurotoxicity. Longitudinal studies are needed to examine long-term influences of these genetic variants on neurobehavior.
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