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We propose activation of G6PD via a small-molecule chaperone as a strategy to increase endogenous defense against bilirubin-induced oxidative stress and prevent kernicterus

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GSSG: no longer provides antioxidant protection must be recycled back into GSH to be useful again reflects how much oxidative stress the body is under High levels of oxidized glutathione signal high internal stress , not high glow

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This was achieved through disruption of the cell cycle and triggering of apoptosis by EgKI-1 whereas, rTsCRT interacted with scavenger receptors [75, 186]