| pubmed-article:3922881 | pubmed:abstractText | In order to explain the mechanism of enhancing effect of irradiation on IL-2 production, assumption that radio-induced free radicals could act as a signal for mitogenesis and/or increase lipid peroxidation of T lymphocyte membrane phospholipids was made. Thus, production of metabolites of the lipoxygenase pathway in the arachidonic acid (AA) cascade, known to increase T cell proliferation and lymphokine production could be enhanced by irradiation. We have shown that (1) hydroxyl radical scavenger (DMSO) abolished IL-2 production, (2) inhibitor of the lipoxygenase pathway (NDGA) strongly decreased IL-2 production, (3) thin layer chromatography demonstrated a polar metabolite(s) of AA in increasing amounts according to the following order: non-irradiated resting cells, non-irradiated stimulated cells, irradiated resting cells, and irradiated stimulated cells. Investigations are in progress to identify this metabolite. | lld:pubmed |
