Brain region-specific deficit in mitochondrial electron transport chain complexes in children with autism

Abha Chauhan, Feng Gu, Musthafa M. Essa, Jerzy Wegiel, Kulbir Kaur, William Ted Brown, Ved Chauhan

Research output: Contribution to journalArticle

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Abstract

Mitochondria play important roles in generation of free radicals, ATP formation, and in apoptosis. We studied the levels of mitochondrial electron transport chain (ETC) complexes, that is, complexes I, II, III, IV, and V, in brain tissue samples from the cerebellum and the frontal, parietal, occipital, and temporal cortices of subjects with autism and age-matched control subjects. The subjects were divided into two groups according to their ages: Group A (children, ages 4-10 years) and Group B (adults, ages 14-39 years). In Group A, we observed significantly lower levels of complexes III and V in the cerebellum (p <0.05), of complex I in the frontal cortex (p <0.05), and of complexes II (p <0.01), III (p <0.01), and V (p <0.05) in the temporal cortex of children with autism as compared to age-matched control subjects, while none of the five ETC complexes was affected in the parietal and occipital cortices in subjects with autism. In the cerebellum and temporal cortex, no overlap was observed in the levels of these ETC complexes between subjects with autism and control subjects. In the frontal cortex of Group A, a lower level of ETC complexes was observed in a subset of autism cases, that is, 60% (3/5) for complexes I, II, and V, and 40% (2/5) for complexes III and IV. A striking observation was that the levels of ETC complexes were similar in adult subjects with autism and control subjects (Group B). A significant increase in the levels of lipid hydroperoxides, an oxidative stress marker, was also observed in the cerebellum and temporal cortex in the children with autism. These results suggest that the expression of ETC complexes is decreased in the cerebellum and the frontal and temporal regions of the brain in children with autism, which may lead to abnormal energy metabolism and oxidative stress. The deficits observed in the levels of ETC complexes in children with autism may readjust to normal levels by adulthood.

Original languageEnglish
Pages (from-to)209-220
Number of pages12
JournalJournal of Neurochemistry
Volume117
Issue number2
DOIs
Publication statusPublished - Apr 2011

Fingerprint

Autistic Disorder
Electron Transport
Brain
Temporal Lobe
Cerebellum
Frontal Lobe
Oxidative stress
Electron Transport Complex III
Occipital Lobe
Parietal Lobe
Oxidative Stress
Mitochondria
Lipid Peroxides
Free Radicals
Adenosine Triphosphate
Energy Metabolism
Tissue
Apoptosis
Age Groups
Observation

Keywords

  • Autism
  • Electron transport chain complexes
  • Energy
  • Mitochondria
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Brain region-specific deficit in mitochondrial electron transport chain complexes in children with autism. / Chauhan, Abha; Gu, Feng; Essa, Musthafa M.; Wegiel, Jerzy; Kaur, Kulbir; Brown, William Ted; Chauhan, Ved.

In: Journal of Neurochemistry, Vol. 117, No. 2, 04.2011, p. 209-220.

Research output: Contribution to journalArticle

Chauhan, Abha ; Gu, Feng ; Essa, Musthafa M. ; Wegiel, Jerzy ; Kaur, Kulbir ; Brown, William Ted ; Chauhan, Ved. / Brain region-specific deficit in mitochondrial electron transport chain complexes in children with autism. In: Journal of Neurochemistry. 2011 ; Vol. 117, No. 2. pp. 209-220.
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