Response of biological markers of the lipid peroxidation process induced by free radical overproduction in rat lung and liver: in vivo and in vitro studies
(1995)
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- Authors
- Supervisors
- Lauwerys, Robert R.
- Abstract
- Free radical overproduction has been proposed as a mechanism of action for several pneumotoxic chemicals. Oxidative degradation of biological membranes has been considered as a possible process by which free radicals mediate lung injury. For some free radical producing chemicals, however, there is indication that the above process may be the consequence rather than the cause of the tissue damage. Whatever the exact significance of oxidative degradation of biological membranes on the sequence of events leading to cellular lesions, it might be of interest to detect its occurrence in workers exposed to pollutants likely to stimulate free radical production in the lung. Therefore, the present study was initiated to assess the response of biological indicators of lipid peroxidation following lung injury induced by free radicals in rats. For comparative purpose, free radical overproduction was also induced in the liver. The principal results can be summarized as follows : <BR> - the monitoring of three markers of lipid peroxidation (ethane in air exhaled, conjugated dienes and TBA-RS in tissues) indicates that the in vivo production of ethane is clearly different following free radical induced damage in lung or liver tissues. Indeed, by using ferrous ions as free radical inducer, lung or liver injuries are associated with lipid peroxidation as evidenced by tissue accumulation of conjugated dienes and TBA-RS but increased ethane exhalation only occurs following peroxidative degradation of liver membranes. <BR> - No evidence for an in vivo peroxidation process of lung membranes is found following intratracheal instillation of paraquat or PMA whereas, as expected interperitoneal injection of CC1 4 results in increased ethane production and conjugated diene formation in liver tissue. <BR> These results led is toundertake in vitro studies aiming at a comparison of the lipid peroxidation process induced in liver and lung tissues submitted to an identical oxidative process. We have also attempted to identify the main determinants of the different response of both tissues<BR> - In vitro, peroxidation of lung and liver homogenates induced by ferrous ions is associated with an increases ethane and TBA-RS production. However, compared to the liver, lung tissue seems to be more resistant to the development of a lipid peroxidation process. <BR> - In vitro, oxygen inhibits ethane formation from both peroxidizing lung an liver tissues but stimulated the production of TBA-RS <BR> - Iron-stimulated peroxidation of pure docosahexaenoic acid preparations leads to a lower accumulation of TBA-RS under air than in the presence of 100% oxygen. However, under the latter condition, no increase in ethane production is formed but ethanol accumulates in the incubation medium. <BR> - Isolated membranes from the lung are more resistant to ferrous ion-induced lipid peroxidation than liver membranes confirming the above observations on tissue homogenates. <BR> - Differences in fatty acid profile could be not account for the different susceptibility of lung and liver microsomes to peroxidative damage. <BR> - The higher vitamin E content in the lung compared to the liver can explain, at least partly, the different resistance of both tissues to an oxidative stress. <BR> On the basis of these in vivo and in vitro studies, it can be concluded that ethane is not an appropriate marker for monitoring a lipid peroxidation process in well-oxygenated tissues such as the lung. The quenching of ethyl radical (the precursor of ethane) by oxygen seems to be an attractive hypothesis to explain the inhibitory effect of oxygen on ethane formation. Our results also suggest that compared to the liver, lung tissue is resistant to the development of lipid peroxidation partly because of its vitamin E content.
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Citations
Schweich, M. D. (1995). Response of biological markers of the lipid peroxidation process induced by free radical overproduction in rat lung and liver: in vivo and in vitro studies. https://hdl.handle.net/2078.5/111309