The reduction in cellular GSH levels results in a concomitant increase in circulating HNE [37]. HNE can be catabolized to acetyl-CoA, propionyl-CoA, and formate through β-oxidation [38]. The increase in HNE and its catabolic intermediates can result in increased cytotoxicity.
Therefore, during oxidative stress, the level of reactive lipid electrophiles becomes so high that the cell is unable to compensate with detoxification mechanisms and, as a result