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Such mutations are frequently observed in clinical isolates as a consequence of the intensive antibiotic therapy to which these isolates are subjected [212]

This process not only directly generates excessive ROS by initiating the non-enzymatic Fenton reaction but also enhances the activity of lipoxygenase (ALOX) or EGLN prolyl hydroxylases (also known as PHD) [1, 19, 20]

J Biol Chem 275: 1077210778 [DOI] [PubMed] [Google Scholar] Sangwan V., Paliouras G.N., Abella J.V., Dube N., Monast A., Tremblay M.L., et al
doi: 10.1093/humrep/deaa363 39
