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PUFAs, particularly AA and adrenergic acid, are susceptible to oxidation owing to the weak C-H bonds in their diallyl group (Kagan et al., 2017)

Coupled with endogenous reactive oxygen species (ROS) generated as by-products of various cellular processes, strict regulation of antioxidants is critical to maintaining a balanced reduction/oxidation (redox) state

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To evaluate whether mutants deficient in different glutathione-dependent enzymes are impacted by TMHT, we subjected cytosolic glutaredoxin mutants to TMHT (Figure 4C)