Cited by 209Autism Spectrum Disorder ResearchGut microbiota and healthTryptophan and brain disorders

Etiology of autistic features: the persisting neurotoxic effects of propionic acid

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El-Ansary, Afaf K, Bacha, Abir Ben, Kotb, Malak·2012·Journal of Neuroinflammation

Abstract

BACKGROUND: Recent clinical observations suggest that certain gut and dietary factors may transiently worsen symptoms in autism. Propionic acid (PA) is a short chain fatty acid and an important intermediate of cellular metabolism. Although PA has several beneficial biological effects, its accumulation is neurotoxic. METHODS: Two groups of young Western albino male rats weighing about 45 to 60 grams (approximately 21 days old) were used in the present study. The first group consisted of oral buffered PA-treated rats that were given a neurotoxic dose of 250 mg/kg body weight/day for three days, n = eight; the second group of rats were given only phosphate buffered saline and used as a control. Biochemical parameters representing oxidative stress, energy metabolism, neuroinflammation, neurotransmission, and apoptosis were investigated in brain homogenates of both groups. RESULTS: Biochemical analyses of brain homogenates from PA-treated rats showed an increase in oxidative stress markers (for example, lipid peroxidation), coupled with a decrease in glutathione (GSH) and glutathione peroxidase (GPX) and catalase activities. Impaired energy metabolism was ascertained through the decrease of lactate dehydrogenase and activation of creatine kinase (CK). Elevated IL-6, TNFα, IFNγ and heat shock protein 70 (HSP70) confirmed the neuroinflammatory effect of PA. Moreover, elevation of caspase3 and DNA fragmentation proved the pro-apoptotic and neurotoxic effect of PA to rat pups CONCLUSION: By comparing the results obtained with those from animal models of autism or with clinical data on the biochemical profile of autistic patients, this study showed that the neurotoxicity of PA as an environmental factor could play a central role in the etiology of autistic biochemical features.

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  1. Chance B Catalases and peroxidases, part II Special methods. Methods Biochem Anal 1954 1 408 13193536

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Authors
El-Ansary, A. K., Bacha, A. B., & Kotb, M.
Affiliations
  • King Saud University (SA)
  • University of Cincinnati (US)
Corresponding author
El-Ansary, Afaf K
Venue
Journal of Neuroinflammation
Published
2012-04-24
Volume
9
Issue
1
Pages
74-74
ISSN
1742-2094 (ISSN-L)
OpenAlex
W2061631433
Cited by
209
References
59
Citations by year
2026: 5 · 2025: 14 · 2024: 13 · 2023: 22 · 2022: 25 · 2021: 19 · 2020: 20 · 2019: 15 · 2018: 19 · 2017: 7 · 2016: 13 · 2015: 9 · 2014: 14 · 2013: 11 · 2012: 3
FWCI
6.07
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
King Saud University
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
autism spectrum disorder, propionic acid, neurotoxicity, short-chain fatty acids, oxidative stress, lipid peroxidation, glutathione, neuroinflammation, apoptosis, caspase-3, energy metabolism, gut dysbiosis, dietary factors, animal models of autism
MeSH terms
Animals, Autistic Disorder, Brain, Disease Models, Animal, Male, Propionates, Random Allocation, Oxidative Stress, Rats

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