Cited by 265Autism Spectrum Disorder ResearchGenetics and Neurodevelopmental DisordersChild Nutrition and Feeding Issues

Evidence of Toxicity, Oxidative Stress, and Neuronal Insult in Autism

Kern, Janet K., Jones, Anne M.·2006·Journal of Toxicology and Environmental Health, Part B

Abstract

According to the Autism Society of America, autism is now considered to be an epidemic. The increase in the rate of autism revealed by epidemiological studies and government reports implicates the importance of external or environmental factors that may be changing. This article discusses the evidence for the case that some children with autism may become autistic from neuronal cell death or brain damage sometime after birth as result of insult; and addresses the hypotheses that toxicity and oxidative stress may be a cause of neuronal insult in autism. The article first describes the Purkinje cell loss found in autism, Purkinje cell physiology and vulnerability, and the evidence for postnatal cell loss. Second, the article describes the increased brain volume in autism and how it may be related to the Purkinje cell loss. Third, the evidence for toxicity and oxidative stress is covered and the possible involvement of glutathione is discussed. Finally, the article discusses what may be happening over the course of development and the multiple factors that may interplay and make these children more vulnerable to toxicity, oxidative stress, and neuronal insult.

Integrity signals

Registry

Crossref · 10.1080/10937400600882079

Cites

166 of 166 references verified0 citation errors · 0 not checkable

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  • Accumulating evidence suggests that a common feature in autism cases may be oxidative stress, the mechanism through which environmental factors exert deleterious effects, which may be exacerbated by interaction of genetically susceptible alleles.

    “Accumulating evidence suggests that a common feature in autism cases may be oxidative stress, the mechanism through which environmental factors exert their deleterious effects, which may be further exacerbated by the interaction of genetically susceptible alleles [96–100].”

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Authors
Kern, J. K., & Jones, A. M.
Affiliations
The University of Texas Southwestern Medical Center (US)
Corresponding author
Kern, Janet K.
Venue
Journal of Toxicology and Environmental Health, Part B
Published
2006-01
Volume
9
Issue
6
Pages
485-499
ISSN
  • 1093-7404 (ISSN-L)
  • 1521-6950
OpenAlex
W2093575302
Cited by
265
References
167
Citations by year
2026: 2 · 2025: 13 · 2024: 6 · 2023: 7 · 2022: 11 · 2021: 13 · 2020: 13 · 2019: 8 · 2018: 10 · 2017: 5 · 2016: 14 · 2015: 14 · 2014: 14 · 2013: 16 · 2012: 17
FWCI
9.06
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Toxicology and Environmental Health Part B (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Health Sciences › Medicine › Psychiatry and Mental health › Child Nutrition and Feeding Issues
Keywords
autism spectrum disorder, oxidative stress, neurotoxicity, neuronal cell death, Purkinje cell degeneration, brain volume, glutathione, environmental risk factors, neurodevelopmental vulnerability
MeSH terms
Autistic Disorder, Brain, Cephalometry, Child, Child, Preschool, Glutathione, Humans, Infant, Infant, Newborn, Organ Size, Purkinje Cells, Lipid Peroxidation, Cell Death, Oxidative Stress, Metals, Heavy

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