Abstract
SummaryBackgroundCoronary artery disease (CAD) is one of the most important causes of mortality and morbidity in wide world population. Dyslipidemia, inflammation and oxidative stress may contribute to disruption of endothelium structure and function, atherosclerosis and CAD. Our study was aimed to determine whether Cu/Zn superoxide dismutase (Cu/Zn SOD) and Mn superoxide dismutase (Mn SOD) gene expression could be modulated by oxidative stress in CAD patients.MethodsThis study included 77 CAD patients and 31 apparently healthy persons. Serum lipid levels, high sensitivity C-reactive protein (hsCRP), total antioxidant status (TAS) and thiobarbituric acid-reacting substances (TBARS) were measured. SOD isoenzymes gene expression was determined in peripheral blood mononuclear cells using quantitative polymerase chain reaction.ResultsMn SOD messenger ribonucleic acid (mRNA) levels were significantly lower in CAD patients than in controls (p=0.011), while Cu/Zn SOD mRNA levels did not change significantly between tested groups (p=0.091). We found significantly lower high-density lipoprotein-cholesterol (HDL-c) (p<0.001) and TAS (p<0.001) levels and significantly higher hsCRP (p=0.002) and TBARS (p<0.001) in CAD patients than in controls. There were significant positive correlations between TAS and Mn SOD mRNA (ρ=0.243, p=0.020) and TAS and Cu/Zn SOD mRNA (r=0.359, p<0.001). TBARS negatively correlated only with Cu/Zn SOD mRNA (ρ=-0.215, p=0.040). TAS levels remained independent predictor for Mn SOD mRNA levels (OR=2.995, p=0.034).ConclusionsResults of this study showed that Mn SOD gene expression were decreased in CAD patients compared to controls and can be modulated by non-enzymatic antioxidant status in blood.
Highlights
Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality in the world [1]
Results of this study showed that Mn superoxide dismutase (Mn superoxide dismutase (SOD)) gene expression were decreased in CAD patients compared to controls and can be modulated by nonenzymatic antioxidant status in blood
Increased total cholesterol (TC) concentrations, especially low-density lipoprotein cholesterol (LDL-c), high triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-c) levels in plasma, are unique factors that are sufficient to lead to atherosclerosis development [4]
Summary
Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality in the world [1]. Atherosclerosis, as chronic inflammatory, fibroproliferative disease of the large and middle-sized arteries is the essential for onset and development of CAD [2]. Dyslipidemia, chronic low-grade inflammation and the imbalance between the production of reactive oxygen species (ROS) and enzymatic and non-enzymatic antioxidant protection could cause endothelial dysfunction of coronary arteries [3,4,5]. Increased total cholesterol (TC) concentrations, especially low-density lipoprotein cholesterol (LDL-c), high triglyceride (TG) and low high-density lipoprotein cholesterol (HDL-c) levels in plasma, are unique factors that are sufficient to lead to atherosclerosis development [4]. Hyperlipidemia stimulates the proinflammatory monocytes to migrate to atherosclerotic lesions where they synthesize large amounts of cytokines and other proinflammatory mediators. Modified lipoproteins interact with scavenger receptors and induce proinflammatory signals within macrophages and foam cells formation [2, 5]
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