Ozden Serin

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 spectrophotometric 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, Hcy 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.

Plasma leptin levels in obese and non-obese postmenopausal women before and after hormone replacement therapy

OBJECTIVE the aim of this study was to investigate the effect of hormone replacement therapy (HRT) on plasma leptin levels in postmenopausal women, and the relationship between the plasma leptin levels and obesity. METHODS premenopausal women with normal cycles (n=30; mean ages, 35.4+/-8.3 years) and postmenopausal women (n=45; mean ages, 49.5+/-4.7 years) were randomly selected. Women were classified as obese (BMI>27 kg/m(2)) and as non-obese (BMI<27 kg/m(2)). Blood samples were obtained from the premenopausal women at the beginning of cycle, and from the postmenopausal women before and 6 months after HRT. Plasma leptin levels were measured by radioimmunassay. RESULTS plasma leptin levels were significantly higher in premenopausal women than in postmenopausal women (18. 60+/-5.0; 3.67+/-2.44 ng/ml, respectively, P<0.001). Obese premenopausal women (n=15) had significantly higher plasma leptin levels (24. 60+/-7.81 ng/ml) in comparison with the levels of the non-obese premenopausal women (n=15; 12.50+/-4. 63 ng/ml) (P<0.001). Although there was no significant difference in the plasma leptin levels between obese (n=25) and non-obese (n=20) postmenopausal women before HRT, plasma leptin levels were significantly elevated in both obese and non-obese postmenopausal women after HRT (P<0.001), and the obese women had significantly higher plasma leptin levels than the non-obese (29.05+/-10.53; 14.78+/-6.76 ng/ml, respectively, P<0.001). CONCLUSION HRT is effective in the elevation of the plasma leptin levels in postmenopausal women, and in obese women the increase of the plasma leptin levels are more marked than the non-obese women after HRT.

Effects of hormone replacement therapy on plasma nitric oxide and total thiol levels in postmenopausal women.

Improvement in endothelial function may be an important mechanism by which hormone replacement therapy (HRT) protects postmenopausal women against coronary artery disease. Our aim was to assess the effects of HRT on plasma nitric oxide (NOx) (nitrate plus nitrite) and total thiols in postmenopausal women, as these parameters are associated with enhanced endothelial functions. Thirty-five healthy postmenopausal volunteers (mean age 50.5 +/- 4.7 yr) in an academic and hospital research environment were involved in the study. Blood samples were collected, one at baseline and the second after 6 mo of HRT. Plasma NOx and total thiol levels were significantly elevated in the subjects after HRT. NOx may be of importance in the protective effects of HRT. Further, the increase of plasma antioxidant thiol levels might also contribute to the beneficial effects of HRT.Improvement in endothelial function may be an important mechanism by which hormone replacement therapy (HRT) protects postmenopausal women against coronary artery disease. Our aim was to assess the effects of HRT on plasma nitric oxide (NOx) (nitrate plus nitrite) and total thiols in postmenopausal women, as these parameters are associated with enhanced endothelial functions. Thirty-five healthy postmenopausal volunteers (mean age 50.5 ± 4.7 yr) in an academic and hospital research environment were involved in the study. Blood samples were collected, one at baseline and the second after 6 mo of HRT. Plasma NOx and total thiol levels were significantly elevated in the subjects after HRT. NOx may be of importance in the protective effects of HRT. Further, the increase of plasma antioxidant thiol levels might also contribute to the beneficial effects of HRT.

Erratum: Interleukin-33, matrix metalloproteinase-9, and tissue inhibitor of matrix metalloproteinase-1 in myocardial infarction

Background/Aims Acute coronary syndrome (ACS) is characterized by increased inflammatory processes and endothelial activation. We investigated the association between ACS and inflammatory mediators and matrix-degrading enzymes. Methods We prospectively enrolled 55 consecutive patients with ACS: 25 with unstable angina (UA) and 30 with non-ST elevated myocardial infarction (NSTEMI). For comparison, 25 age- and sex-matched subjects with no significant coronary artery stenosis were included as the control group. Peripheral serum levels of interleukin (IL)-33, matrix metalloproteinase (MMP)-9, tissue inhibitor of MMP-1, and C-reactive protein (CRP) were measured on admission, and at 12, 24, 48, and 72 hours after the initial evaluation. Results Compared to serum levels in the control group, serum levels of IL-33 decreased in the NSTEMI group (p < 0.05), and levels of MMP-9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 increased in the UA group (p < 0.01, p < 0.05, respectively) and NSTEMI group (p < 0.05, p < 0.05, respectively). IL-33 levels were significantly lower on admission than at 12 hours after the initial evaluation (p < 0.05). IL-33 levels were negatively correlated with MMP-9 levels (r = -0.461, p < 0.05) and CRP levels (r = -0.441, p < 0.05). Conclusions Elevated levels of MMP-9, TIMP-1, and decreased levels of IL-33 play a role in the development and progression of ACS.