Evaluation of Oxidative Stress Parameters and Antioxidant Status in Coronary Artery Disease Patients.

A surge in oxidative stress and weakened antioxidant defense contributes to the initiation and progression of Coronary Artery Diseases (CAD). The resultant burst in free radicals causes oxidation of lipoproteins mainly oxidized low-density lipoprotein (oxLDL). Further studies need to be conducted to find whether the management of CAD can be evaluated within the context of oxidant/antioxidant balance with the contribution of newer markers. This study was performed to evaluate, compare, and correlate oxidative stress parameters and antioxidant status in CAD patients with controls and evaluate and compare pro-oxidant, a pro-inflammatory enzyme, myeloperoxidase (MPO) and anti-oxidant, anti-inflammatory enzyme, and paraoxonase (PON) between CAD patients and controls. OxLDL, an oxidation product of low-density lipoprotein, malondialdehyde (MDA), an oxidative marker, and reduced glutathione (GSH), an anti-oxidant marker, and lipid profile were assessed and compared in CAD patients and controls. The activity of MPO was correlated with that of PON, and MDA level was correlated with GSH level. A total of 100 clinically proven CAD patients, in the age range of 35-70 years, were selected from the Out Patient Department (OPD) of our Institute. A total of 60 controls in the same age range and without CAD were selected after undergoing health checkups in the hospital. Based on the obtained results, oxLDL, MDA, and MPO were significantly increased in patients than in controls (<0.05), and PON and GSH were significantly lowered in patients than in controls (<0.05). Total cholesterol, triglyceride, and LDL were significantly high in CAD patients. A significant negative correlation was observed between MPO and PON levels and between MDA and GSH levels. Increased oxidative stress and decreased antioxidant status were observed in patients with CAD. Formation of oxLDL increased MPO and decreased PON are all additional risk factors for the development of CAD and can be targeted for future therapeutic purposes. Lifestyle modifications and treatment methods can reduce CAD risk through the reduction of oxidative stress and improvement of antioxidant status.