ArticleToxicology and applied pharmacology2005
Developmental consequences of in utero sodium arsenate exposure in mice with folate transport deficiencies.
Article in Toxicology and applied pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Comparing Folic Acid Interventions and Arsenic Reduction Strategies for Neural Tube Defect Prevention in Bangladesh: A Systematic Review and Decision Analysis.Birth defects research · 2025Pooled it
- Folate and arsenic metabolism: a double-blind, placebo-controlled folic acid-supplementation trial in Bangladesh.The American journal of clinical nutrition · 2006Trial
- Nutrition, one-carbon metabolism and arsenic methylation.Toxicology · 2021Review
- Impact of prenatal arsenate exposure on gene expression in a pure population of migratory cranial neural crest cells.Reproductive toxicology (Elmsford, N.Y.) · 2019Article
- Nutritional Influences on One-Carbon Metabolism: Effects on Arsenic Methylation and Toxicity.Annual review of nutrition · 2018Review
- Does arsenic increase the risk of neural tube defects among a highly exposed population? A new case-control study in Bangladesh.Birth defects research · 2017Article
- Polymorphisms in maternal folate pathway genes interact with arsenic in drinking water to influence risk of myelomeningocele.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Physical, chemical, and biological methods for the removal of arsenic compounds.BioMed research international · 2014Review
- Role of folic Acid on symptoms of chronic arsenic toxicity.International journal of preventive medicine · 2014Article
- Genetic and epigenomic footprints of folate.Progress in molecular biology and translational science · 2012Review
- Nutritional manipulation of one-carbon metabolism: effects on arsenic methylation and toxicity.Journal of toxicology · 2012Article
- Gene expression profiling in the fetal cardiac tissue after folate and low-dose trichloroethylene exposure.Birth defects research. Part A, Clinical and molecular teratology · 2010Article
- Arsenate-induced apoptosis in murine embryonic maxillary mesenchymal cells via mitochondrial-mediated oxidative injury.Birth defects research. Part A, Clinical and molecular teratology · 2010Article
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
Abstract
Previous studies have demonstrated that mice lacking a functional folate binding protein 2 gene (Folbp2-/-) were significantly more sensitive to in utero arsenic exposure than were the wild-type mice similarly exposed. When these mice were fed a folate-deficient diet, the embryotoxic effect of arsenate was further exacerbated. Contrary to expectations, studies on 24-h urinary speciation of sodium arsenate did not demonstrate any significant difference in arsenic biotransformation between Folbp2-/- and Folbp2+/+ mice. To better understand the influence of folate pathway genes on arsenic embryotoxicity, the present investigation utilized transgenic mice with disrupted folate binding protein 1 (Folbp1) and reduced folate carrier (RFC) genes. Because complete inactivation of Folbp1 and RFC genes results in embryonic lethality, we used heterozygous animals. Overall, no RFC genotype-related differences in embryonic susceptibility to arsenic exposure were observed. Embryonic lethality and neural tube defect (NTD) frequency in Folbp1 mice was dose-dependent and differed from the RFC mice; however, no genotype-related differences were observed. The RFC heterozygotes tended to have higher plasma levels of S-adenosylhomocysteine (SAH) than did the wild-type controls, although this effect was not robust. It is concluded that genetic modifications at the Folbp1 and RFC loci confers no particular sensitivity to arsenic toxicity compared to wild-type controls, thus disproving the working hypothesis that decreased methylating capacity of the genetically modified mice would put them at increased risk for arsenic-induced reproductive toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.