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[31] In response to the accumulation of the hazardous metabolic byproducts of aerobic respiration, biological systems evolved various strategies to counteract O 2 toxicity

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Copper and CuNPs have the ability to stimulate apoptosis by caspase-dependent and independent pathways through induction of pro-apoptotic protein (Bax) and suppression of anti-apoptotic protein (Bcl-2) [66, 90, 96], while chrysin activates apoptosis through intrinsic pathways of apoptosis in view of p53 and Bak, caspase-9 and caspase-3 enhancement, and Bcl2 downregulation [96]

Multisystem physiological perspective of human frailty and its modulation by physical activity