The role of reactive oxygen species, cytokines and cytochrome P450 in pulmonary damage due to hyperoxia
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Mechanistic role of cytochrome P450 (CYP)1B1 in oxygen-mediated toxicity in pulmonary cells: A novel target for prevention of hyperoxic lung injury
2016, Biochemical and Biophysical Research CommunicationsCitation Excerpt :CYP is a family of heme-containing proteins that are involved in the metabolism of numerous endogenous substrates and xenobiotics [9]. Induction of CYP1A by β-naphtoflavone (BNF) or 3-methylcholanthrene (MC) prior to hyperoxia protects mice and rats against the toxic effects of oxygen exposure [10,11]. Meanwhile, pre-treatment of rats with a CYP1A inhibitor, aminobenzotriazole, followed by exposure to 95% O2 leads to severe inflammation, pleural effusions, and severe lung injury [12].
Immunocytochemical study of cytochrome P450 (1A1/1A2) induction in murine ocular tissues
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2016, Mini-Reviews in Medicinal ChemistryPlace of iron chelators like desferrioxamine and deferasirox in management of hyperoxia-induced lung injury; a systematic review
2010, International Journal of PharmacologyControl of Bcl-2 expression by reactive oxygen species
2003, Proceedings of the National Academy of Sciences of the United States of America
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