These phase I oxidative reactions metabolise 210% of paracetamol to a reactive intermediate, N -acetyl- p -benzoquinone imine (NAPQI) which mediates the hepatotoxic effect of paracetamol
Arabidopsis chloroplastic glutaredoxin C5 as a model to explore molecular determinants for iron-sulfur cluster binding into glutaredoxins
demonstrated that regulatory B (Breg) cells play a critical role in resolving Pseudomonas aeruginosa -induced pneumonia [1]
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Additionally, oxamate-induced LDHA inhibition promoted ROS accumulation and ATP depletion, causing DNA damage, impairing DNA repair, and improving radiotherapy efficacy in NSCLC [345]
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