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While the above evidence indicates that the mitochondrial apoptotic pathway promotes cell death, recent provocative evidence has shown that the intrinsic apoptosis pathway mediates the pro-longevity response to mitochondrial ROS in Caenorhabditis elegans by triggering a unique pattern of gene expression that modulates stress sensitivity and promotes survival (Yee et al., 2014)

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The % inhibition of DPPH free-radicals scavenging activities of the standards was 51.63, 64.11, 87.52, and 55.47% with an IC 50 value of 9.1 0.01 g/mL, 4.9 0.02 g/mL, 1.8 0.001 g/mL, 1.4 0.02 g/mL, respectively

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Importantly, 5FU-based combination treatment also shows an increase in mitochondrial mass (FOLFOX (5FU + 1 M oxaliplatin) or FOLFIRI (5FU + 5 nM SN38, active metabolite of irinotecan)) that we attribute to 5FU-imposed stress, given that single-agent oxaliplatin or SN38 do not promote the same degree of mitochondrial adaptation (Extended Data Fig

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