CIGARETTE-SMOKE BLOCKS CROSS-LINKING OF ELASTIN INVITRO
- 1 January 1983
- journal article
- research article
- Published by Elsevier
- Vol. 127 (2) , 189-192
- https://doi.org/10.1164/arrd.1983.127.2.189
Abstract
Water-soluble components of the gas phase of filtered cigarette smoke inhibit formation of covalent desmosine cross-links during conversion of tropoelastin to elastin in vitro. These same smoke components also suppress lysyl-oxidase-catalyzed oxidation of lysine .epsilon.-amino groups in tropoelastin (the chemical step preceding formation of all elastin cross-links, including desmosine) in a dose-dependent fashion. Gas phase smoke does not block the oxidation of diaminopentane by lysyl oxidase. Gas phase cigarette smoke may possess substrate-directed (rather than enzyme-directed) inhibitory components capable of interfering with elastin cross-linking in vitro. Similar effects occurring in [human] smokers'' lungs could impede elastin repair and contribute to the development of pulmonary emphysema.This publication has 3 references indexed in Scilit:
- Potential mechanism of emphysema: alpha 1-proteinase inhibitor recovered from lungs of cigarette smokers contains oxidized methionine and has decreased elastase inhibitory capacity.Proceedings of the National Academy of Sciences, 1982
- Control of elastin metabolism by elastin ligands. Reciprocal effects on lysyl oxidase activity.Journal of Biological Chemistry, 1981
- Desmosine Radioimmunoassay for Measuring Elastin DegradationIn Vivo1–3American Review of Respiratory Disease, 1980