M A Bhat1, G Gandhi1. 1. a Department of Human Genetics , Guru Nanak Dev University , Amritsar , India.
Abstract
OBJECTIVE: The objective of the present study was to evaluate oxidative DNA damage in peripheral blood leukocytes (PBLs) of patients with coronary artery disease (CAD) and to explore the relationship of oxidised purine and pyrimidine with oxidative stress. METHODS: The study participants (n = 100) included 50 patients and unrelated 50 age-, sex- and population-subgroup (Jat Sikhs)-matched healthy controls. Oxidative DNA damage using the modified enzymatic comet in PBLs, and malondialdehyde (MDA) levels, total oxidant status (TOS) and total antioxidant status (TAS) in blood serum samples using spectrophotometric methods was determined. RESULTS: The basal DNA damage of percent tail DNA (T-DNA%) was increased as were tail moment (TM) and olive tail moment (OTM). Oxidative DNA damage in terms of oxidised purines and oxidised pyrimidines was also significantly (p < .001) elevated in patients. Rather the advanced stages of CAD, unstable angina and acute myocardial infarction had significantly more basal and oxidative DNA damage (p < .05) compared to stable angina. MDA levels (p < .01) and TOS (p < .001) were increased significantly in patients with significant (p < .001) decrease in TAS. There was positive correlation of oxidised purines (T-DNA% r = 0.399, p = .004; TM r = 0.623, p = .001; OTM r = 0.456, p= .001) and of total oxidative damage (TM r = 0.515, p = .001; OTM r = 0.463, p = .001) with disease severity, and, with TOS (r = 0.279, p = .050) and negative with TAS (r = -0.341, p = .015). Multiple linear regression analysis revealed TOS and disease severity as independent predictors of oxidative DNA damage. CONCLUSIONS: There was significant increase in oxidative DNA damage and oxidative stress in CAD patients compared to levels in healthy controls.
OBJECTIVE: The objective of the present study was to evaluate oxidative DNA damage in peripheral blood leukocytes (PBLs) of patients with coronary artery disease (CAD) and to explore the relationship of oxidised purine and pyrimidine with oxidative stress. METHODS: The study participants (n = 100) included 50 patients and unrelated 50 age-, sex- and population-subgroup (Jat Sikhs)-matched healthy controls. Oxidative DNA damage using the modified enzymatic comet in PBLs, and malondialdehyde (MDA) levels, total oxidant status (TOS) and total antioxidant status (TAS) in blood serum samples using spectrophotometric methods was determined. RESULTS: The basal DNA damage of percent tail DNA (T-DNA%) was increased as were tail moment (TM) and olive tail moment (OTM). Oxidative DNA damage in terms of oxidised purines and oxidised pyrimidines was also significantly (p < .001) elevated in patients. Rather the advanced stages of CAD, unstable angina and acute myocardial infarction had significantly more basal and oxidative DNA damage (p < .05) compared to stable angina. MDA levels (p < .01) and TOS (p < .001) were increased significantly in patients with significant (p < .001) decrease in TAS. There was positive correlation of oxidised purines (T-DNA% r = 0.399, p = .004; TM r = 0.623, p = .001; OTM r = 0.456, p= .001) and of total oxidative damage (TM r = 0.515, p = .001; OTM r = 0.463, p = .001) with disease severity, and, with TOS (r = 0.279, p = .050) and negative with TAS (r = -0.341, p = .015). Multiple linear regression analysis revealed TOS and disease severity as independent predictors of oxidative DNA damage. CONCLUSIONS: There was significant increase in oxidative DNA damage and oxidative stress in CAD patients compared to levels in healthy controls.