T-786C single-nucleotide polymorphism (SNP) of endothelial nitric oxide synthase gene and serum level of vascular endothelial relaxant factor (VERF) in non-diabetic patients with coronary artery disease

Various mutations on endothelial nitric oxide synthase (eNOs) gene cause reduced production of NO, a vascular endothelial relaxant factor (VERF), and may accelerate the process of atherosclerosis. The study was designed to investigate the frequency of T-786C polymorphism of the gene in patients suffering from coronary artery disease (CAD) in North West of Iran. One hundred and twenty (120) subjects including 60 patients with angiographically diagnosed CAD and 60 age and sex matched CAD-free subjects as control were studied. The levels of nitric oxide in the samples were measured with the Griess Method. The genotype studies were carried using allele specific PCR. Compared with the control, reduced levels of NO were noticed in the patient group (p < 0.05) and significantly high frequency of eNOs -786C genotype was found in CAD patients (p < 0.05). The low levels of NO and increased frequency of T-786C polymorphism might be a risk factor in the progression of coronary artery disease in the studied subjects.Key words: Coronary artery disease, endothelial nitric oxide synthase gene, T-786C SNP, vascular endothelial relaxant factor, non-diabetic

Association between nucleotide mutation of eNOS gene and serum level of vessel expansion factor (VEF) in non-smoker patients with vascular heart disease

Various mutation on endothelial nitric oxide synthase (eNOs) gene cause reduced production of NO, the expansion factor (VEF) and may accelerate the process of atherosclerosis. The study was designed to investigate the frequency of T-786C polymorphism of the gene or nucleotide mutation of eNOS gene in patients suffering from vascular heart disease (VHD) or coronary artery disease (CAD) in North West of Iran. 120 subjects including 60 patients with angiographically diagnosed CAD and 60 age and sex matched CAD-free subjects as control were studied. The levels of Nitric oxide in the samples were measured with the Griess method. The genotype studies were carried out using allele specific PCR. Comparing with the control reduced levels of NO were noticed in the patient group (P<0.05) and significantly high frequency of eNOs -786C genotype was found in CAD patients (P<0.05). The low levels of NO and increased frequency of T-786C polymorphism might be a risk factor in progression of coronary artery disease in the studied subjects.Keywords: Vascular heart disease, endothelial nitric oxide synthase gene, TC 786 SNP, vessel expansion factor (VEF), non-smokerAfrican Journal of Biotechnology Vol. 12(20), pp. 3023-302

Association of OX-LDL and MDA Serum Level with Extent of Coronary Artery Disease

Background: Atherosclerosis is the main reason of Coronary Artery Disease (CAD). The studies show that several factors are interconnected with the development and progression of CAD including lipid peroxidation, inflammation and homeostasis. The aim of this study was to evaluate the serum level of Oxidized LDL (OX-LDL) and Malondialdehyde (MDA) and their association with the extent of Coronary Artery Disease. Methods: In this cross-sectional study serum OX-LDL and MDA levels were determined in 160 patients with Coronary Artery Disease comprised of 40 subjects with no vessel disease, 40 subjects with single vessel disease, 40 subjects with double vessel disease, and 40 subjects with triple vessel disease matched control healthy 20 subjects. Serum levels of OX-LDL determined used to (ELISA) procedure. Serum level of MDA was measured by photometric method based on reaction with Thiobarbituric Acid (TBA). Data were analyzed using Spearman correlation coefficients, Student's t test or ANOVA. Result: Oxidized LDL and Malondialdehyde serum levels in patient groups were significantly higher than control groups (p<0.05). Furthermore, serum concentrations of OX-LDL in double-vessel disease were significantly higher as compare with control and no-vessel groups and triple vessel disease were significantly higher as compare with single vessel disease (p<0.05). Serum concentrations of MDA in double-vessel disease were significantly higher as compare with control and no-vessel groups and triple vessel disease were significantly higher as compare with single vessel disease (p<0.05). Conclusion: Elevated serum levels of OX-LDL and MDA indicate potential role in atherogenesis leading to CAD. There for our findings suggest that determination of serum OX-LDL and MDA levels can be useful as diagnostic and monitoring markers in patients with CAD and its extent

Study on the relation between the levels of trace elements and minerals with cardiac ventricular rupture in rats

Background: This study aimed to examine whether the copper-deficient rat might be a model for cardiac ventricular rupture in humans.Materials and Methods: Male weanling rats were fed diets that were adequate (5.7 mg/kg diet) or deficient (0.3 mg/kg diet) in copper for 49 days, and 24 of the copper- deficient rats died of cardiac rupture. The autopsy samples of heart and liver were obtained from rats who died of cardiac rupture or controls who died of noncardiac causes. Results: Trace element measurements indicated that organ copper concentration was reduced by copper-deficiency in rats, the manganese concentration in organs of copper- deficient rats was higher than that of the controls. Iron concentration was lower in the rats with the ruptured hearts and not different in the ruptured copper-deficient hearts compared to the controls and liver iron concentration was higher than controls in copper deficiency and was not different from controls in rats with cardiac rupture. Macromineral measurements indicated that: magnesium concentration was lower in ruptured hearts of copper-deficient rats than it was in their respective controls phosphorus was elevated in both sets of ruptured hearts, as was sodium and calcium concentration in ruptured hearts of copper-deficient rats was higher than in controls.Conclusion: The trace element changes, especially for copper, are not associated with cardiac rupture in rats, but similar macromineral changes associated with rupture in copper-deficient rats probably reflect the common endpoint of both conditions, tissue necrosis