Elsevier

Medical Hypotheses

Volume 34, Issue 4, April 1991, Pages 296-299
Medical Hypotheses

The role of reactive oxygen species, cytokines and cytochrome P450 in pulmonary damage due to hyperoxia

https://doi.org/10.1016/0306-9877(91)90045-ZGet rights and content

Abstract

The exact mechanism of hyperoxic damage and the (therapeutic) protection against these lesions are still a matter of debate. Recent experimental studies indicated a role for cytokines, cytochrome P450, and antioxidant enzymes in protection against O2 toxicity. In this paper a hypothesis is presented linking all these factors to cytochrome P450 oxidase as a central enzyme.

References (20)

There are more references available in the full text version of this article.

Cited by (10)

  • 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 Communications
    Citation 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].

  • Induction of cytochrome P450 1A1 and 1A2 by hyperoxia

    1993, Biochemical and Biophysical Research Communications
  • Disulfiram’s anticancer activity: Evidence and mechanisms

    2016, Mini-Reviews in Medicinal Chemistry
  • Control of Bcl-2 expression by reactive oxygen species

    2003, Proceedings of the National Academy of Sciences of the United States of America
View all citing articles on Scopus
View full text