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Gliomas harboring IDH1 mutations have been reported to have a decreased ability to compensate for reactive oxygen species (ROS) (9), due to reduced IDH1-wildtype activity and concomitant low nicotinamide adenine dinucleotide phosphate (NADPH) (10)

Dihydroartemisinin@MIL-101 nanoreactor produces ROS and consumes GSH, resulting in the accumulation of lipid peroxide and induction of ferroptosis in lung cancer (Lewis) cells [188]

This analysis indicates that gpx-1 (ortholog of human GPX4) RNAi leads to variable lifespan extension relative to wild-type controls and exhibits non-additive lifespan extension with fard-1(oe) (Figure 5figure supplement 1C)

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The CDS of CPC was expressed under the control of pCPC (-686 to -158)