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NADPH contributes to recycling in oxidized antioxidant systems involving glutathione, thioredoxins, glutaredoxins, and peroxiredoxins and maintains another reactive oxygen species (ROS)-detoxifying enzyme, catalase, in its active form, suggesting that the homeostatic level of G6PD-derived NADPH determines the rate of oxidative damage [8]

Additionally, the FOXO4-p53 interaction contributes to the maintenance of senescent cells by activating the transcription of their common target gene, p21cip1, which suppresses apoptosis 36

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Apart from oxidative stress, As also inhibits photosynthesis by damaging the chloroplast [227]