[Lipid peroxidation in bronchoalveolar lavage fluid in interstitial lung diseases in relation to other components and smoking].
ABSTRACT We measured lipid peroxide (LPO) in bronchoalveolar lavage fluid (BALF) from patients with interstitial lung diseases (ILD, 45 cases) including sarcoidosis (22 cases) and idiopathic interstitial pneumonia (7 cases). LPO correlated negatively with the macrophage fraction, and positively with lymphocyte fraction, type III procollagen N terminal peptide (PIIIP), and total protein in all cases. In sarcoidosis, it correlated with PIIIP positively, and in IIP, with total cell count, macrophage count, PIIIP/protein and total protein. Comparison between the current smoker group (SM) and non-smoker group (NON/EX) showed that in all cases, SM had lower LPO, lymphocyte fraction, lymphocyte count and total protein whereas higher macrophage fraction than NON/EX. In sarcoidosis, SM had a lower lymphocyte fraction and total protein and higher macrophage fraction. We conclude that LPO in BALF reflects inflammation and fibrosis occurring in the lung with ILD and this process might be suppressed in smokers.
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ABSTRACT: Cigarette smoke contains a large variety of compounds, including many oxidants and free radicals that are capable of initiating or promotes oxidative damage. Also, oxidative damage may result from reactive oxygen species generated by the increased and activated phagocytes following cigarette smoking. In vitro studies are generally supportive of the hypothesis that cigarette smoke can initiate or promote oxidative damage. However, information obtained from in vivo studies is inconclusive. Contrary to expectations, the levels of lipid peroxidation products were found to be decreased or unchanged in the lungs of chronically smoked rats. Metabolic adaptation, such as accumulation of vitamin E in the lung, and increased activities of superoxide dismutase in alveolar macrophages and pulmonary tissues of chronically smoked animals may enable smoked subjects to counteract oxidative stress and to resist further damage to smoke exposure. However, it is also possible that the metabolic adaptation may be secondary to inflammatory response and injury repair process following smoking exposure. More studies are needed to better understand the role of oxidative damage in the etiology of smoking-related disorders.Annals of the New York Academy of Sciences 06/1993; 686:289-98. DOI:10.1111/j.1749-6632.1993.tb39189.x · 4.31 Impact Factor