Evaluation of the relationship between haptoglobin polymorphisms with antioxidant enzymes activity in patients with coronary heart disease

Abstract

BackgroundAtherosclerosis, the most common pathologic process underlying cardiovascular disease, defines a state of intensified oxidative stress and impaired antioxidative capacity. Haptoglobin (Hp) polymorphisms include three distinct human genotypes (Hp1-1, Hp2-1, and Hp2-2), managing functional differences related to the risk of developing cardiovascular diseases. The present study proposed to examine Haptoglobin polymorphisms concerning antioxidative enzyme activity in patients with coronary artery disease. MethodsThis case-control inquiry was managed through 398 samples consisting of 225 men and 173 women aged 30–80 who were suspect of CAD. Patients were classified as CAD cases (255) and controls (143). Hp genotyping was conducted using a polymerase chain reaction (PCR). Total antioxidant capacity (TAC) was examined using the Ferric Reducing Ability of Plasma (FRAP) method, and Erythrocyte CAT and GPx activity were measured as antioxidant enzymes. ResultsThe TG, Chol/HDL, diabetes, GPx enzyme, and FRAP results demonstrate a meaningful variation in patients than controls (p > 0.005). The frequency of haptoglobin polymorphisms was significantly different between patients compared to controls. The frequency of Hp genotypes had a significant association with the severity of vascular stenosis so that the Hp2 allele increased the probability of vascular stenosis (P = 0.03).GPx enzyme activity presented a significant difference in Hp2-2 compared to Hp2-1 and Hp1-1 patients. However, there were no notable variations between the Hp genotypes and the amount of catalase and total antioxidant capacity (p > 0.005). ConclusionThis examination confirms that antioxidative enzyme activities are Hp-phenotype-dependent in coronary artery disease. Impaired GPx enzyme activities were prominent among coronary artery disease patients with Hp2-2. Besides, diabetic and high BMI patients with Hp2-2 genotype possess a higher prevalence of coronary artery disease. This study proves the HP2 allele as a genetic determinant in controlling oxidative stress in CAD patients.