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Etiology of autistic features: the persisting neurotoxic effects of propionic acid
Open accessAbstract
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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“In animal models, for example, propionate (although directly administered to the brain intracerebroventricularly or in high concentrations) can induce autism-like behaviors (366, 367)”
From Diet and the Microbiota–Gut–Brain Axis: Sowing the Seeds of Good Mental Health (2021) · cites this paper as [367]
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Metadata
- 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
- ORCID
- El-Ansary, Afaf K
- Venue
- Journal of Neuroinflammation
- Published
- 2012-04-24
- Volume
- 9
- Issue
- 1
- Pages
- 74-74
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3425128
- 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
- gold
- doi.org
- 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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