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Glutathione and ABC transporters as determinants of sensitivity to oxidative and nitrosative stress.

The development of novel drugs remains a high priority in the successful therapeutic management of cancer. We have applied our accumulated knowledge of the importance of glutathione (GSH), glutathione S-transferases (GSTs), and ATP-dependent binding cassette (ABC) transporters to the identification of novel targets and testing of new agents that are influenced by thiol homeostasis in tumors. Glutathione S-transferase π (GST π ) interacts with and suppresses the activity of c-Jun NH 2 terminal kinase (JNK) (1). GST π -deficient mice (GST π −/− ) have higher levels of circulating white blood cells than wild type mice. A peptidomimetic inhibitor of GST π disrupts the interaction between GST π and JNK and mimics in wild type mice the increased myeloproliferation observed in GST π −/− mice. In an in vitro hematopoiesis assay, interleukin-3, granulocyte-colony stimulating factor, and granulocyte-macrophage-colony stimulating factor were more effective at stimulating proliferation of hematopoietic cells in GST π −/− mice than in wild type mice. The GST π inhibitor increased myeloproliferation induced by these cytokines in wild type but not in GST π −/− mice, suggesting a key role for GST π in the effect of this drug. The JNK inhibitor, SP600125 which itself caused little inhibition of cytokine-induced myeloproliferation, prevented all myelostimulant effects of the GST π