Abstract
Background Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation, abnormal permanent distal air-space enlargement and emphysema in the lungs. Increased oxidative burden in COPD is because of both directly a result of smoking and indirectly by the release of increasing amount of ROS from airways leukocytes. The CYP1A1 gene modifies the phase I enzyme aryl hydrocarbon hydroxylase (AHH) belonging to the cytochrome P450 system that plays a major role in the metabolism of exogenous toxins generated by cigarette smoke [1]. The aim of the present study is to assess the role of CYP1A1 gene polymorphism and to measure the plasma nitric oxide levels in the etiology of COPD in South Indian Population from Andhra Pradesh.
Highlights
Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation, abnormal permanent distal air-space enlargement and emphysema in the lungs
There is an increased frequency of CC genotype and C allele in the COPD patients compared to control subjects (X2 = 4.51; p=0.03; OR=1.94; 95% CI = (1.044-3.605) and (X2=5.12; p=0.02; OR=1.35; 95% CI=(1.041-1.758). (Table 1)
The study carried out from North Indian population have shown that CYP1A1,3801 polymorphism was significantly associated with COPD [2]
Summary
Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation, abnormal permanent distal air-space enlargement and emphysema in the lungs. TC and 6.8% of CC in control subjects (Figure 1). There is an increased frequency of CC genotype and C allele in the COPD patients compared to control subjects (X2 = 4.51; p=0.03; OR=1.94; 95% CI = (1.044-3.605) and (X2=5.12; p=0.02; OR=1.35; 95% CI=(1.041-1.758).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have