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MECHANISM OF 4-HYDROXYNONENAL INDUCED TOXICITY IN JURKAT CD4+ T LYMPHOCYTES Wei-Yuan Chang April 24, 2006 Oxidative stress-induced immunosuppression could be due to a decrease in CD4+ T lymphocyte activation or proliferation. 4-Hydroxynonenal (HNE), an end product of lipid peroxidation, and its protein adducts act as markers of oxidative stress. In this study, the effects of HNE on a human CD4+ Jurkat T cells were examined. Systematic determinations of the effects of HNE on cytotoxicity, Akt and protein phosphatase 2A(PP2A)activation, FaslFasL-mediated apoptotic signaling, methionine adenosyltransferase (MAT) II activity, MAT 2A and c-Myb expression and cellular glutathione (GSH) and S-adenosylmethionine (SAMe) levels were performed. The results showed that HNE induced cytotoxicity, downregulated Akt and upregulated PP2A activation, and resulted in enhanced FasL expression, death-inducing signaling complex (DISC) formation, Fas-associated death domain (FADD) recruitment, and caspases cleavages, and comitantiy decreased c-FLIPs expression. Further, HNEinduced cytotoxicity and lost of survival is associated with GSH depletion in a threshold phenomena and can be potentiated by inhibition of GSH synthesis. In addition, HNE toxicity was also involved with SAMe metabolism by inhibition of MAT II activity, MAT 2A and c-Myb expression and which resulted in decreases in

Mechanism of 4-Hydroxynonenal induced toxicity in Jurkat CD4+ T lymphocytes.