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Protection is likely mediated by redox activation of the AMPK and NRF2 pathways

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This oxidant stress causes activation of a MAP kinase cascade in the cytosol ultimately leading to phosphorylation of c-jun N-terminal kinase (P-JNK), translocation of P-JNK to the mitochondria [34], and binding to the anchor protein Sab [35] for amplification of the mitochondrial oxidant stress and peroxynitrite formation in the mitochondrial matrix [33, 36]