HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hukkanen, J. Articles by Raunio, H. Search for Related Content PubMed PubMed Citation Articles by Hukkanen, J. Articles by Raunio, H.

Expression of xenobiotic-metabolizing enzymes in human pulmonary tissue: possible role in susceptibility for ILD

¹ Dept of Pharmacology and Toxicology, University of Oulu, Oulu, and ² University of Kuopio, Kuopio, Finland

CORRESPONDENCE: O. Pelkonen, Dept of Pharmacology and Toxicology, University of Oulu, POB 5000, FIN-90014, Oulu, Finland. Fax: 358 85375247

Keywords: cytochrome P450, cytochrome P450 enzymes, xenobiotic-metabolizing enzymes

Received: March 8, 2001
The studies in the authors' laboratories have been financially supported by the Academy of Finland and the Biomed2 programme (EUROCYP Project).

The lung is a major target for all inhaled toxicants. Many inhaled chemicals are not hazardous as such, but are biotransformed to reactive intermediates. Therefore, the pathogenesis of interstitial and other lung diseases is intimately linked to exposure to environmental and other chemicals, which may be causative or modifying factors in the cellular pathways and mechanisms mediating oxidative stress and cell protection in the pulmonary tissue.

Several different xenobiotic-metabolizing cytochrome P450 (CYP) and phase II enzymes (i.e. conjugation enzymes including several transferases) are present in the human lung and lung-derived cell lines, possibly contributing to in situ activation and inactivation of chemical toxicants. This paper describes the expression and localization of individual CYP-forms in the lung.

Interindividual differences in the expression of these enzymes may contribute to the risk of developing interstitial and other lung diseases initiated by agents that require metabolic activation.