Intracellular and extracellular redox status and free radical generation in primary immune cells from children with autism

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Intracellular and extracellular redox status and free radical generation

in primary immune cells from children with autism.

<http://www.ncbi.nlm.nih.gov/pubmed/22928106>

Rose S, Melnyk S, Trusty TA, Pavliv O, Seidel L, Li J, Nick T, SJ.

Autism Res Treat. 2012;2012:986519

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.