INTRODUCTION: Oxidative and nitrosative stress caused by a disturbance in the homeostasis of pro-oxidants and antioxidants play a vital role in the pathogenesis of coronary heart disease (CHD). Enhanced formation of reactive oxygen species/reactive nitrogen species may also affect the oxidation/nitration of biomolecules such as lipids, proteins and DNA. The present study was undertaken to estimate oxidative and nitrosative stress, and to evaluate oxidative DNA damage. METHODS: The study population consisted of 120 patients with angiographically documented CHD and an equal number of age- and gender-matched healthy controls. Lipid profiles were estimated using Glaxo kits. Estimation of plasma malondialdehyde (MDA), nitrite/nitrate and comet assay were carried out using previously published methods. RESULTS: Lipid profiles were significantly different in patients with coronary artery disease compared to the controls (p-value less than 0.01). The levels of MDA, nitrite/nitrate and DNA damage in the patients were significantly higher compared to the controls, and a strong correlation was found between the comet tail length and the MDA and nitrite/nitrate levels. Further analysis revealed that the influence of nitrite/nitrate was greater than that of MDA. CONCLUSION: Our results indicate that abnormal levels of lipid profiles, along with increased oxidative and nitrosative stress as well as somatic DNA damage, could be important pathogenic factors that act as additional prognostic predictors. They may also serve as potential targets for therapeutic strategies in CHD for early management and prevention of the disease.
INTRODUCTION: Oxidative and nitrosative stress caused by a disturbance in the homeostasis of pro-oxidants and antioxidants play a vital role in the pathogenesis of coronary heart disease (CHD). Enhanced formation of reactive oxygen species/reactive nitrogen species may also affect the oxidation/nitration of biomolecules such as lipids, proteins and DNA. The present study was undertaken to estimate oxidative and nitrosative stress, and to evaluate oxidative DNA damage. METHODS: The study population consisted of 120 patients with angiographically documented CHD and an equal number of age- and gender-matched healthy controls. Lipid profiles were estimated using Glaxo kits. Estimation of plasma malondialdehyde (MDA), nitrite/nitrate and comet assay were carried out using previously published methods. RESULTS:Lipid profiles were significantly different in patients with coronary artery disease compared to the controls (p-value less than 0.01). The levels of MDA, nitrite/nitrate and DNA damage in the patients were significantly higher compared to the controls, and a strong correlation was found between the comet tail length and the MDA and nitrite/nitrate levels. Further analysis revealed that the influence of nitrite/nitrate was greater than that of MDA. CONCLUSION: Our results indicate that abnormal levels of lipid profiles, along with increased oxidative and nitrosative stress as well as somatic DNA damage, could be important pathogenic factors that act as additional prognostic predictors. They may also serve as potential targets for therapeutic strategies in CHD for early management and prevention of the disease.