ArticleBrain and behavior2020
Fetal exposure to dichloroacetic acid and impaired cognitive function in the adulthood.
Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Associations between Maternal Urinary Metabolite Concentrations of Selected Volatile Organic Compounds and Child Neurocognitive Development at Two Years of Age.Environmental health perspectives · 2025Article
- Effect and mechanism of Dichloroacetate in the treatment of stroke and the resolution strategy for side effect.European journal of medical research · 2025Review
- Three-dimensional diffractive acoustic tomography.Nature communications · 2025Article
- Fetal exposure to dichloroacetic acid and impaired cognitive function in the adulthood.Brain and behavior · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
introductionDichloroacetic acid (DCA), a by-product of disinfection in drinking water, is a multiple organ carcinogen in humans and animals. Still, little research on its neurotoxicity and its underlying mechanism has not been elucidated.
methodsSprague Dawley rats were intragastrically treated with DCA at 10, 30, 90 mg/kg body weight from pregnancy till delivery. At eight weeks of age of pups, we assessed cognitive performance using the standard behavioral tests. And the hippocampus structure and ultrastructure were evaluated using light and electron microscope. The oxidative stress indicators and neuroinflammation factors were measured with the corresponding kits. The mRNA and protein of synaptic factors were detected using RT-PCR and Western blot.
resultsThe results indicated that maternal weight gain and offspring birthweight were not significantly affected by DCA. However, behavioral tests, including morris water maze and step down, showed varying degrees of changes in DCA-treated pups. Additionally, we found significant differences in hippocampal neurons by histomorphological observation. Biochemical analysis results indicated superoxide dismutase (SOD) and catalase (CAT) activities, as well as reactive oxygen species (ROS), nitric oxide (NO), and reduced glutathione (GSH) levels, were affected by DCA accompanying with DNA damage. Moreover, the results showed that the neuroinflammation factors (TNF-α, IL-6, IL-1β) in DCA treatment groups increased significantly compared with the control pups. And we also found that DCA treatment caused a differential modulation of proteins (BDNF, cAMP-response element-binding protein1 (CREB1), p-CREB1, postsynaptic density-95 (PSD-95), synapsin I, p-synapsin I), and mRNA (BDNF, PSD-95).
conclusionsTaken together, these results above showed that oxidative stress, neuroinflammation response, and weakened synaptic plasticity in pups hippocampus induced by fetal exposure to DCA could damage the function of memory and cognition in the adulthood.
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