Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain
Open accessAbstract
Despite increasing evidence of oxidative stress in the pathophysiology of autism, most studies have not evaluated biomarkers within specific brain regions, and the functional consequences of oxidative stress remain relatively understudied. We examined frozen samples from the cerebellum and temporal cortex (Brodmann area 22 (BA22)) from individuals with autism and unaffected controls (n=15 and n=12 per group, respectively). Biomarkers of oxidative stress, including reduced glutathione (GSH), oxidized glutathione (GSSG) and glutathione redox/antioxidant capacity (GSH/GSSG), were measured. Biomarkers of oxidative protein damage (3-nitrotyrosine; 3-NT) and oxidative DNA damage (8-oxo-deoxyguanosine; 8-oxo-dG) were also assessed. Functional indicators of oxidative stress included relative levels of 3-chlorotyrosine (3-CT), an established biomarker of a chronic inflammatory response, and aconitase activity, a biomarker of mitochondrial superoxide production. Consistent with previous studies on plasma and immune cells, GSH and GSH/GSSG were significantly decreased in both autism cerebellum (P<0.01) and BA22 (P<0.01). There was a significant increase in 3-NT in the autism cerebellum and BA22 (P<0.01). Similarly, 8-oxo-dG was significantly increased in autism cerebellum and BA22 (P<0.01 and P=0.01, respectively), and was inversely correlated with GSH/GSSG in the cerebellum (P<0.01). There was a significant increase in 3-CT levels in both brain regions (P<0.01), whereas aconitase activity was significantly decreased in autism cerebellum (P<0.01), and was negatively correlated with GSH/GSSG (P=0.01). Together, these results indicate that decreased GSH/GSSG redox/antioxidant capacity and increased oxidative stress in the autism brain may have functional consequence in terms of a chronic inflammatory response, increased mitochondrial superoxide production, and oxidative protein and DNA damage.
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Oxidative stress and reduced redox/antioxidant capacity in cerebellum and temporal cortex have functional consequences for chronic inflammatory response, mitochondrial dysfunction, and protein and DNA damage.
“Oxidative stress and reduced redox/antioxidant capacity in cerebellum and temporal cortex have been shown to have functional consequences for chronic inflammatory response, mitochondrial dysfunction and protein and DNA damage [3], and in peripheral tissue have been associated with anti-neuronal positivity [16] and clinical features of autism [15].”
From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [3]
Several lines of evidence indicate oxidative stress and mitochondrial dysfunction are prevalent in individuals with ASD.
“There are presently several lines of evidence indicating oxidative stress and mitochondrial dysfunction are prevalent in individuals with ASD [3,10,11,12,13,14,15,16].”
From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [3]
Children with ASD have elevated levels of pro-inflammatory cytokines including IL-6, TNF-α, and IFN-γ in different tissues.
“Furthermore, evidence suggests that children with ASD have elevated levels of pro-inflammatory cytokines including, interleukin 6 (IL–6), tumour necrosis factor alpha (TNF–α), and interferon gamma (IFN-γ) in different tissues [3,4,5,6,7].”
From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [3]
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Self-citation
- Authors
- Rose, S., Melnyk, S., Pavliv, O., Bai, S., Nick, T. G., Frye, R. E., & James, S. J.
- Affiliations
- Arkansas Children's Hospital (US)
- Corresponding author
- Rose, S
- Venue
- Translational Psychiatry
- Published
- 2012-07-10
- Volume
- 2
- Issue
- 7
- Pages
- e134-e134
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC3410618
- OpenAlex
- W2113675370
- Cited by
- 480
- References
- 69
- Citations by year
- 2026: 25 · 2025: 40 · 2024: 39 · 2023: 36 · 2022: 41 · 2021: 33 · 2020: 43 · 2019: 29 · 2018: 31 · 2017: 30 · 2016: 32 · 2015: 27 · 2014: 39 · 2013: 32 · 2012: 3
- FWCI
- 16.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (unspecified)
- Locations
- Translational Psychiatry (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Center for Research Resources (UL1RR024148)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD051873)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- autism spectrum disorder, oxidative stress, glutathione redox state, reduced glutathione, glutathione disulfide, cerebellum, temporal cortex, nitrotyrosine, 8-hydroxy-2'-deoxyguanosine, 3-chlorotyrosine, aconitase activity, mitochondrial superoxide, oxidative DNA damage, oxidative protein damage, neuroinflammation, brain biomarkers
- MeSH terms
- Aconitate Hydratase, Autistic Disorder, Cerebellum, Chromatography, High Pressure Liquid, Glutathione, Humans, Inflammation, Oxidation-Reduction, Temporal Lobe, Tyrosine, Biomarkers, Linear Models, Case-Control Studies, Oxidative Stress
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