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Previous studies indicated that lysosomal iron is released and translocated into the mitochondria contributing to MPT in APAP-induced injury ( 2+ uniporter MCFU plays a key role in APAP-induced oxidative stress, mitochondrial dysfunction, and hepatocellular death ( 2+ from lysosomes followed by uptake into mitochondria via MCFU is a key mechanism in APAP-mediated hepatotoxicity

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To this end, 32D cells, a mouse myeloid progenitor line which proliferation is dependent on interleukin-3 (IL-3) 26 , were employed for WT- and T315I-Bcr-Abl transformation