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Oxidative or nitrosative stress induced by physiological or pathological conditions leads to a decreased ratio of GSH/GSSG

204 Similarly, administration of the PRMT5 inhibitor PJ-68 in a CML mouse model with high expression of PRMT5 LSCs could deplete DVL3, thereby inhibiting Wnt/-catenin signaling and significantly prolonging the survival time of a retroviral BCR-ABL-driven CML mouse model

The relative amounts of each form determine the cellular redox status (GSH/GSSG ratio) which is often used as a marker of antioxidative capacity of cells [2]

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