Oxidants and Antioxidants in COPD Associated with Tobacco Smoke and Biomass Exposure

Abstract

BACKGROUND Chronic Obstructive Pulmonary Disease (COPD) is one of the leading causes of chronic morbidity and mortality. Apart from tobacco smoke, biomass fuel has been implicated as an important etiological factor for development of COPD. Oxidantantioxidant imbalance is known to play a key role in pathophysiology of COPD. The study was undertaken to evaluate the role of oxidative stress and antioxidant status among COPD cases due to tobacco smoking and biomass exposure. METHODS Serum MDA, and erythrocyte SOD and GSH levels, were estimated among 40 COPD cases due to tobacco smoking (Group 1), 20 COPD cases due to biomass exposure (Group 2). 40 age and sex matched healthy controls (Group 0) were also included. Serum MDA, SOD and GSH were measured calorimetrically by TBA method, Marklund & Marklund method and method by Beutler et al respectively. RESULTS IBM SPSS Ver. 20 was used for statistical analysis and preparation of tables. Significantly higher levels of MDA were seen among COPD cases due to tobacco smoke (58.08±52 vs 15.3705±6.6; p value <0.01) compared to controls. SOD levels were significantly lower in both case groups compared to controls (1123.3±301.2, 1147.01±200.5 vs 1315.23±209.1; p value<0.01). GSH levels were lower in tobacco smoking group when compared to biomass exposed group (7.98±2.7 vs 9.61±2.1; p value 0.01). Positive correlation was found between FEV1% and SOD in group 1 cases. CONCLUSIONS The results support the hypothesis of presence of increased oxidative stress and oxidant-antioxidant imbalance in pathogenesis of COPD. It plays an important role in disease severity which is higher among COPD in tobacco smokers compared to biomass exposed COPD.

Systematic Review and Meta-Analysis of the Blood Glutathione Redox State in Chronic Obstructive Pulmonary Disease

“…Of them, 1340 were excluded because they were either irrelevant or duplicates. After a full-text review of the remaining 48 articles, a further 30 were excluded, as they did not meet the inclusion criteria, leaving the remaining 18 for further analysis [ 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 ]. The retrieved studies were published between 2002 and 2019, and their characteristics are described in Table 1 .…”

“…The mean age ranged between 42.0 and 75.7 years in the COPD patients and between 43.7 and 77.7 years in the controls. The blood concentrations of reduced GSH (rGSH) were measured in 14 studies [ 34 , 35 , 36 , 37 , 39 , 40 , 41 , 42 , 44 , 45 , 46 , 47 , 48 , 49 ], while total GSH (tGSH) was measured in four studies [ 32 , 33 , 38 , 43 ]. GSH was measured in red blood cells (RBCs) in nine studies and in whole blood (WB) in the other nine.…”

“…The GSH concentrations were reported as the median and IQR, mean and SE, and mean and standard deviation. COPD was diagnosed according to the GOLD guidelines in nine articles [ 33 , 37 , 38 , 42 , 43 , 44 , 45 , 46 , 48 ], the ATS/ERS guidelines in two studies [ 41 , 47 ] and the BTS guidelines in one study [ 34 ]. Six studies did not report the guidelines used for COPD diagnosis [ 32 , 35 , 36 , 39 , 40 , 49 ].…”

“…When compared to healthy controls, the blood (RBCs/WB) rGSH concentrations in COPD patients were significantly lower in 10 studies [ 34 , 35 , 36 , 39 , 41 , 44 , 45 , 46 , 47 , 49 ], significantly higher in one study [ 48 ], and non-significantly different in the remaining three studies [ 37 , 40 , 42 ]. A forest plot of the blood rGSH concentrations in COPD patients vs. healthy subjects is presented in Figure 2 .…”