Oxidative stress in autism
Open accessAbstract
Autism is a severe developmental disorder with poorly understood etiology. Oxidative stress in autism has been studied at the membrane level and also by measuring products of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants involved in the defense system against reactive oxygen species (ROS). Lipid peroxidation markers are elevated in autism, indicating that oxidative stress is increased in this disease. Levels of major antioxidant serum proteins, namely transferrin (iron-binding protein) and ceruloplasmin (copper-binding protein), are decreased in children with autism. There is a positive correlation between reduced levels of these proteins and loss of previously acquired language skills in children with autism. The alterations in ceruloplasmin and transferrin levels may lead to abnormal iron and copper metabolism in autism. The membrane phospholipids, the prime target of ROS, are also altered in autism. The levels of phosphatidylethanolamine (PE) are decreased, and phosphatidylserine (PS) levels are increased in the erythrocyte membrane of children with autism as compared to their unaffected siblings. Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autism. Furthermore, environmental and genetic factors may increase vulnerability to oxidative stress in autism. Taken together, these studies suggest increased oxidative stress in autism that may contribute to the development of this disease. A mechanism linking oxidative stress with membrane lipid abnormalities, inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity, leading to clinical symptoms and pathogenesis of autism is proposed.
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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].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [98]
Glutathione is a significant antioxidant and closely related to detoxification in the brain.
“Glutathione is a significant antioxidant and closely related to detoxification in the brain39.”
From Altered composition and function of intestinal microbiota in autism spectrum disorders: A systematic review (2019) · cites this paper as [39]
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- Authors
- Chauhan, A., & Chauhan, V.
- Corresponding author
- Chauhan, Abha
- Venue
- Pathophysiology
- Publisher
- Elsevier BV
- Published
- 2006-08
- Volume
- 13
- Issue
- 3
- Pages
- 171-181
- ISSN
- 0928-4680 (ISSN-L)
- OpenAlex
- W2128294896
- Cited by
- 656
- References
- 145
- Citations by year
- 2026: 22 · 2025: 27 · 2024: 25 · 2023: 30 · 2022: 35 · 2021: 29 · 2020: 42 · 2019: 27 · 2018: 39 · 2017: 32 · 2016: 32 · 2015: 39 · 2014: 48 · 2013: 44 · 2012: 39
- FWCI
- 12.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Pathophysiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- autism spectrum disorder, oxidative stress, lipid peroxidation, reactive oxygen species, antioxidant enzymes, glutathione, ceruloplasmin, transferrin, erythrocyte membrane phospholipids, phosphatidylethanolamine, phosphatidylserine, superoxide dismutase, glutathione peroxidase, catalase, inflammation, excitotoxicity, mitochondrial dysfunction, immune dysfunction, autism pathogenesis
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