Intracellular and Extracellular Redox Status and Free Radical Generation in Primary Immune Cells from Children with Autism / Shannon ROSE in Autism Research and Treatment, (September 2011)  

Public ISBD [article]  inAutism Research and Treatment > (September 2011) . - 10 p. Titre : Intracellular and Extracellular Redox Status and Free Radical Generation in Primary Immune Cells from Children with Autism Type de document : Texte imprimé et/ou numérique Auteurs : Shannon ROSE, Auteur ; Stepan MELNYK, Auteur ; Timothy A. TRUSTY, Auteur ; Oleksandra PAVLIV, Auteur ; Lisa SEIDEL, Auteur ; Jingyun LI, Auteur ; Todd NICK, Auteur ; S. Jill JAMES, Auteur Année de publication : 2011 Article en page(s) : 10 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The modulation of the redox microenvironment is an important regulator of immune cell activation and proliferation. To investigate immune cell redox status in autism we quantified the intracellular glutathione redox couple (GSH/GSSG) in resting peripheral blood mononuclear cells (PBMCs), activated monocytes and CD4 T cells and the extracellular cysteine/cystine redox couple in the plasma from 43 children with autism and 41 age-matched control children. Resting PBMCs and activated monocytes from children with autism exhibited significantly higher oxidized glutathione (GSSG) and percent oxidized glutathione equivalents and decreased glutathione redox status (GSH/GSSG). In activated CD4 T cells from children with autism, the percent oxidized glutathione equivalents were similarly increased, and GSH and GSH/GSSG were decreased. In the plasma, both glutathione and cysteine redox ratios were decreased in autistic compared to control children. Consistent with decreased intracellular and extracellular redox status, generation of free radicals was significantly elevated in lymphocytes from the autistic children. These data indicate primary immune cells from autistic children have a more oxidized intracellular and extracellular microenvironment and a deficit in glutathione-mediated redox/antioxidant capacity compared to control children. These results suggest that the loss of glutathione redox homeostasis and chronic oxidative stress may contribute to immune dysregulation in autism. En ligne : http://dx.doi.org/10.1155/2012/986519 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=149 [article] Intracellular and Extracellular Redox Status and Free Radical Generation in Primary Immune Cells from Children with Autism [Texte imprimé et/ou numérique] / Shannon ROSE, Auteur ; Stepan MELNYK, Auteur ; Timothy A. TRUSTY, Auteur ; Oleksandra PAVLIV, Auteur ; Lisa SEIDEL, Auteur ; Jingyun LI, Auteur ; Todd NICK, Auteur ; S. Jill JAMES, Auteur . - 2011 . - 10 p. Langues : Anglais (eng) in Autism Research and Treatment > (September 2011) . - 10 p. Index. décimale : PER Périodiques Résumé : The modulation of the redox microenvironment is an important regulator of immune cell activation and proliferation. To investigate immune cell redox status in autism we quantified the intracellular glutathione redox couple (GSH/GSSG) in resting peripheral blood mononuclear cells (PBMCs), activated monocytes and CD4 T cells and the extracellular cysteine/cystine redox couple in the plasma from 43 children with autism and 41 age-matched control children. Resting PBMCs and activated monocytes from children with autism exhibited significantly higher oxidized glutathione (GSSG) and percent oxidized glutathione equivalents and decreased glutathione redox status (GSH/GSSG). In activated CD4 T cells from children with autism, the percent oxidized glutathione equivalents were similarly increased, and GSH and GSH/GSSG were decreased. In the plasma, both glutathione and cysteine redox ratios were decreased in autistic compared to control children. Consistent with decreased intracellular and extracellular redox status, generation of free radicals was significantly elevated in lymphocytes from the autistic children. These data indicate primary immune cells from autistic children have a more oxidized intracellular and extracellular microenvironment and a deficit in glutathione-mediated redox/antioxidant capacity compared to control children. These results suggest that the loss of glutathione redox homeostasis and chronic oxidative stress may contribute to immune dysregulation in autism. En ligne : http://dx.doi.org/10.1155/2012/986519 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=149

Metabolic Imbalance Associated with Methylation Dysregulation and Oxidative Damage in Children with Autism / Stepan MELNYK in Journal of Autism and Developmental Disorders, 42-3 (March 2012)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.367-377 Titre : Metabolic Imbalance Associated with Methylation Dysregulation and Oxidative Damage in Children with Autism Type de document : Texte imprimé et/ou numérique Auteurs : Stepan MELNYK, Auteur ; George J. FUCHS, Auteur ; Eldon SCHULZ, Auteur ; Maya LOPEZ, Auteur ; Stephen G. KAHLER, Auteur ; Jill J. FUSSELL, Auteur ; Jayne BELLANDO, Auteur ; Oleksandra PAVLIV, Auteur ; Shannon ROSE, Auteur ; Lisa SEIDEL, Auteur ; David W. GAYLOR, Auteur ; S. Jill JAMES, Auteur Année de publication : 2012 Article en page(s) : p.367-377 Langues : Anglais (eng) Mots-clés : Autism  Oxidative stress  Metabolic  Epigenetics  Glutathione  DNA methylation Index. décimale : PER Périodiques Résumé : Oxidative stress and abnormal DNA methylation have been implicated in the pathophysiology of autism. We investigated the dynamics of an integrated metabolic pathway essential for cellular antioxidant and methylation capacity in 68 children with autism, 54 age-matched control children and 40 unaffected siblings. The metabolic profile of unaffected siblings differed significantly from case siblings but not from controls. Oxidative protein/DNA damage and DNA hypomethylation (epigenetic alteration) were found in autistic children but not paired siblings or controls. These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression. Further, these results suggest a plausible mechanism by which pro-oxidant environmental stressors may modulate genetic predisposition to autism. En ligne : http://dx.doi.org/10.1007/s10803-011-1260-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152 [article] Metabolic Imbalance Associated with Methylation Dysregulation and Oxidative Damage in Children with Autism [Texte imprimé et/ou numérique] / Stepan MELNYK, Auteur ; George J. FUCHS, Auteur ; Eldon SCHULZ, Auteur ; Maya LOPEZ, Auteur ; Stephen G. KAHLER, Auteur ; Jill J. FUSSELL, Auteur ; Jayne BELLANDO, Auteur ; Oleksandra PAVLIV, Auteur ; Shannon ROSE, Auteur ; Lisa SEIDEL, Auteur ; David W. GAYLOR, Auteur ; S. Jill JAMES, Auteur . - 2012 . - p.367-377. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.367-377 Mots-clés : Autism  Oxidative stress  Metabolic  Epigenetics  Glutathione  DNA methylation Index. décimale : PER Périodiques Résumé : Oxidative stress and abnormal DNA methylation have been implicated in the pathophysiology of autism. We investigated the dynamics of an integrated metabolic pathway essential for cellular antioxidant and methylation capacity in 68 children with autism, 54 age-matched control children and 40 unaffected siblings. The metabolic profile of unaffected siblings differed significantly from case siblings but not from controls. Oxidative protein/DNA damage and DNA hypomethylation (epigenetic alteration) were found in autistic children but not paired siblings or controls. These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression. Further, these results suggest a plausible mechanism by which pro-oxidant environmental stressors may modulate genetic predisposition to autism. En ligne : http://dx.doi.org/10.1007/s10803-011-1260-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152

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