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Glutathione (c-glutamyl-cysteinyl-glycine, GSH), resulting from its reactivity and high intracellular concentrations (up to ten mM in the liver and in different very malignant cells), is involved in several cellular functions. GSH is particularly relevant in cancer cells since it is involved in regulating e.g. carcinogenic mechanisms, development and dissemination, and multidrug and radiation resistance [1,two,3]. A classical model in metastasis research, the very metastatic B16 melanoma F10 (B16-F10), shows larger GSH content, GSH synthesis rate, and decrease GSH efflux than the B16-F1 cell subset with low metastatic prospective [4]. Interleukin 6 (IL-6) (mostly of tumor origin) facilitates GSH release from hepatocytes and its interorgan transport through theblood circulation to increasing metastatic foci in B16-F10-bearing mice [5]. Recently we studied in the event the capacity of metastatic cells to overproduce IL-6 is regulated by cancer cell-independent mechanisms. We discovered that pathophysiological levels of stress-related hormones (corticostero.