Plasma homocysteine levels in obese and non-obese subjects with or without hypertension;: its relationship with oxidative stress and copper

Objectives: The relationship between plasma total Homocysteine (tHcy) and oxidative stress and plasma levels of lipids, insulin and copper levels were investigated in obese and nonobese hypertensives. Design and Methods: Plasma tHcy levels were determined by an enzyme immunoassay method. Plasma lipid peroxidation levels were measured as thiobarbituric acid reactive substances (TBARS) by spectrofotometric methods. Plasma levels of copper and insulin were measured by atomic absorption spectrophotometer and electrochemiluminescence method, respectively. Results: Plasma tHcy, copper and insulin levels did not differ in nonobese hypertensives compared to nonobese normotensives. Plasma TBARS levels were significantly increased in nonobese hypertensives when compared to nonobese normotensives (p < 0.001). Plasma tHcy, TBARS, copper and fasting insulin levels were significantly higher in obese normotensives and hypertensives than in nonobese normotensives and hypertensives, respectively (for each comparison; p < 0.001). There was a significant difference in plasma tHcy, TBARS and copper levels between obese subjects with or without hypertension (for each comparison p < 0.01). The univariate analyses demonstrated a significant positive correlation between tHcy and TBARS (coefficient +/- SE, 0.411 +/- 0.115, p < 0.01) and copper (coefficient +/- SE, 0.425 +/- 0.135, p < 0.01) in obese subjects. In a multivariate regression analysis in obese subjects tHcy was positively correlated with TBARS (coefficient +/- SE, 0.480 +/- 0.155, p < 0.01) and copper (coefficient +/- SE, 0.486 +/- 0.140, P < 0.01). Conclusions: We hypothesize that in the presence of other traditional risk factors, Hey may have a permissive role in the endothelium damage even within the normal range and this role may be related to free radical generating systems. Therefore, modest elevation of plasma Hcy may causally be involved in the pathogenesis of atherosclerosis and/or cardiovascular disease. (C) 2003 The Canadian Society of Clinical Chemists. All rights reserved.