ABSTRACT
Aims: Chronic Obstructive Pulmonary Disease (COPD) is the fourth leading cause of death worldwide. Its prevalence is increasing in the world. Tobacco smoking is the major risk factor for COPD. Oxidant-antioxidant and protease – anti-protease imbalance is the major hallmarks for the pathogenesis of COPD. The present study was planned to assess the correlation between markers of airflow obstruction with the serum level of neutrophil elastase, nitric oxide and superoxide dismutase in COPD patients. Study Design: Case Control Study. Place and Duration of Study: Department of Biochemistry, B. J. Govt. Medical College, Pune [Maharashtra]. The study period was in between Feb.2012 to Dec. 2013. Methodology: Study comprised of 60 stable COPD patients and 60 healthy controls. COPD patients were selected as per the GOLD (Global Initiative for Obstructive Lung Disease) criteria with of aged between 40 to 75 yrs. Each subject undergone through the pulmonary function test by spirometry prior to enter in the study and predicted values of FEV1, FVC and FEV1/FVC were measured. Serum level of neutrophil elastase (NE) was analyzed using commercial available ELISA kits while serum level of nitric oxide and superoxide dismutase were measured by spectrophotometric methods. Statistical analysis was done by using SPSS software 17 version. Results: In our study we observed significantly increased levels of serum neutrophil elastase and nitric oxide and decreased level of enzymatic antioxidant superoxide dismutase (SOD) in COPD patients as compared to healthy controls. We found significant strong inverse correlation between neutrophil elastase (r=-0.604, P<0.0001) and nitric oxide (r=-0.565, P<0.0001) with FEV1% predicted and positive correlation between superoxide dismutase and FEV1% predicted (r=+0.394, P<0.001) in COPD patients. Conclusion: The present study demonstrates that the level of nitric oxide, superoxide dismutase and neutrophil elastase in serum might have played role in oxidative stress and inflammation in COPD patients. Hence, it can be concluded that the measurement of these biomarkers in serum may provide a good approach to assess the severity of the disease in COPD patients.
ABSTRACT
Chronic Obstructive Pulmonary Disorder (COPD) is projected to rank third leading cause of deaths by 2030 as per WHO. COPD is a multietiological disease. The airflow dysfunction is usually progressive, associated with an abnormal inflammatory response of the lungs to noxious particles or gasses. As the lung is exposed to high levels of oxygen, it is more susceptible to oxidants mediated injury. Gender based differences are identifiable risk factors. Smoking is found to be a major risk factor in the causation of COPD resulting in oxidative stress . The aim of the present study is to evaluate the oxidant antioxidant imbalance in healthy non smoker controls and smokers with COPD. A total of 60 control (healthy non smokers) and 121 smokers having COPD were studied. The mean age is more in smoker group as compared to healthy controls, which identifies advancing age as a risk factor for COPD. The mean BMI and weight of smoker group is reduced as compared to control group. GOLD 2008 criteria was used to assess lung functions. Lung functions namely FEV1, FVC, FEV1/FVC% and FEV1% Predicted showed significant reduction in smoker group as compared to healthy non smoker controls. MDA in control and smoker group (1.09±0.09 and 1.41±0.23 nmol/ml respectively) showed significant changes (P<0.001). Our results also demonstrate significant reduction in anti oxidant enzymes namely SOD (units/mg of serum protein), Catalase (units/mg of serum protein) and GPX (nmol of NADPH oxidized/ min/mg of serum protein) in smoker group as compared to healthy controls. On the basis of study it is concluded that smoking, gender and oxidant antioxidant imbalance are identifiable risk factors in COPD.
ABSTRACT
BACKGROUND: It is well known that oxygen free radicals (OFR) play a vital role in the various type of acute lung injury. Among various antioxidant defense mechanisms, the superoxide dismutases (SOD) are thought to be the first line of antioxidant defense by catalyzing the dismutation of two superoxide radicals to yield hydrogen peroxide and oxygen. Eukaryotic cells contain two types of intracellular SOD : cytosolic, dimeric copper/zinc- containing enzyme (CuZnSOD) and mitochondrial, tetrameric manganese-containing enzyme (MnSOD). The purpose of this study is to evaluate the time-dependent gene expression of MnSOD and CuZnSOD in the endotoxin-treated rats, and to compare with the manifestations of LPS-induced acute lung injury in rats. METHODS: Total RNA from rat lung was isolated using single step phenol extraction 0, 1, 2, 4, 6, 12, 18, 24 hours after E. coli endotoxin injection (n=3, respectively). RNA was separated by formaldehyde-containing 1.2% agarose gels elctrophoresis, transblotted, baked, prehybridized, and hybridized with 32P-labeled cDNA probes for rat MnSOD and CuZnSOD, which were kindly donated by Dr. Ho (Duke University, Durham, NC, USA). The probes were labeled by nick translation. Blots were washed and autoradiography were quantitated using laser densitometry. Equivalent amounts of total RNA/gel were assessed by monitoring 285 and 185 rRNA. RESULTS: Endotoxin caused a rise in steady-state MnSOD mRNA levels by 4h with peak mRNA accumulation by 6h. Continued MnSOD mRNA expression was observed at 12h. CuZnSOD mRNA expression was observed from 1h to 24h with peak levels by 18h. CONCLUSION: These results suggest that SOD palys an important defensive role in the endotoxin-induced acute lung injury in rats.