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Increased cellular protein S -glutathionylation sensitized hepatocytes to TNF hepatotoxicity Increased cellular glutathionylated protein levels in response to GSSG accumulation prompted us to examine the effects of cellular protein S -glutathionylation on TNF-induced cell death

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Collectively these studies confirmed the critical role of genes StAR, 3-HSD, Cyp17a, and aromatase along with LC provides as a therapeutic agent to restore toxic damage through normal gene expression

Further longitudinal analyses in initially non-depressed subjects are needed to properly disentangle these two mutually non-exclusive scenarios