Effect of heavy cigarette and water pipe smoking on antioxidants and lipids in Sudanese male smokers: a case-control study

Background: Tobacco smoking is a source of many toxins such as free radicals, mutagenic substances as well as cause for developing cardiovascular diseases (CVD), particularly atherosclerosis. This study aims to assess the impact of smoking on antioxidants in Sudanese male smokers. Methods: Cases were 85 and 48 men who smoke cigarettes (CS) and water pipe (WPS) respectively and they were compared with matching 50 non-smoking controls. Blood samples were collected and following parameters: Glutathione peroxidase, Superoxide dismutase, Total cholesterol, Triglyceride, LDL, HDL, Paraoxinase, and Malondialdehyde were measured. Results: There were no significant differences in biochemical parameters between light CS and WPS compared to controls. In heavy smokers of both WPS and CS, the TC, TG, LDL, and MDA were higher than controls (p>0.05), GPx, SOD, HDL, and PON were lower in smokers than controls (p>0.05). In both groups of smokers, HDL, GPx, SOD, and PON were inversely correlated with duration of smoking (p>0.05), also, HDL was positively correlated with SOD and GPx (p>0.05). Moreover, GPx and SOD were correlated with each other in both groups of smokers (p>0.05). Conclusion: In Sudanese male smokers' biochemical profile disturbances suggest that heavy smoking was leading to developing CVD, particularly WPS

The Increased Expression of Gelatinolytic Proteases Due to Gigarette Smoking Exposure in the Lung of Guinea Pig / 결핵

BACKGROUND: Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality amont the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hyopthesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. METHODS: Two groups of five guinea pigs were exposed to the whole smoke of 20 commerical cigarettes per day, 5 hours/day, 5 days/week, for 6 weeks, and 12 weeks, respectively, using a smoking apparatus. Five agematched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically examined(×400) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at 4℃). Two sets of culture plates were loaded with 1×106 intraalveolar cells. One plate, contained 0.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at 37℃. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. RESULTS: At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field (400×) was 121.4±7.2, 158.0±20.2, 196.8±32.8, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, r2=0.675). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDTA. However, the gelatinolytic enzymes were not expressed in the control groups. CONCLUSION: CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic preoteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of gunea pigs.