study of HyperhomocysteInemIa and CAD In BulgarIan populatIon

study of HyperhomocysteInemIa and CAD In BulgarIan populatIon

There is growing evidences that Homocysteine (Hcy) is an independent risk factor for coronary artery diseases (CAD) and a sensitive marker of Cobalamine and Folate function. In this study total Homocysteine (tHcy), Folate (Fol), Vit. B12, total cholesterol, triglycerides and HDL-C were measured in 89 patients (age 35-65), survived myocardial infarction (MI), and in 70 age and sex matched control subjects. Additionally we have genotyped them for C677T MTHFR polymorphism. Serum tHcy level was determined using automated Abbott IMx fluorescence polarization assay. Fol and B12 were determined using Chemiluminescence ACS:180 assays. We find significantly higher levels of Hcy in patients, compared to controls (18.008.76 mol/L vs. 13.825.94 mol/L , p=0.001). The Fol levels were lower in patients than in controls (13.908.56 nmol/L vs. 21.6411.53 nmol/L, p<0.001). Vit. B12 levels were also lower in patients (96,2796.5 pmol/L vs. 312.8  131.9 pmol/L, p=0.008). Patients were more frequently carriers of T/T genotype, compared to controls (16 vs. 3, p=0.023). After log-transformation of values, the bivariant correlation analysis was performed to estimate the strength of association between Hcy and Fol in different groups. Statistically significant negative correlation (r=-0.359, p=0.001) was find in patients survived MI, but not in control subjects (r=-0.121, p=0.345). The same results were obtained when patients and controls were divided by age.

Our results suggest that high Hcy and low Fol and vit.B12, more frequently found in patients with MI than in controls probably contribute to high cardiovascular disease risk in these patients. C677T MTHFR genotype can in part, but not fully explain high Hcy/low Fol levels.

P59

Selma SÜER GÖKMEN¹, A.Cemal AYGIT², Reyhan YILDIZ¹, Beyhan ÇAKIR², Şendoğan GÜLEN¹

In extrahepatic mammalian tissues, arginase is believed to supply the cell with ornithine, a precursor for biosynthesis of the polyamines. Arginase activity and ornithine level have been shown to be elevated during carcinogenesis. The aim of this study is to determine arginase activity and ornithine level in benignant and malignant skin tumors and, to evaluate whether they can be used as biological markers for distinguishing patients with benignant skin tumors from those with malignant skin tumors. Arginase activity and ornithine level were determined by the method of Geyer and Dabich, and that of Chinard, respectively. The protein content of the tissues was determined by the method of Lowry. One unit of arginase was defined as the amount of enzyme that released 1µmol of urea for 1 minute at 37 ⁰C. The Wilcoxon two-sample test and Student’s t test were used to analyze the results. The mean arginase activity and ornithine levels in benignant tumor tissues were 10.45±3.77 U/mg protein (n=26) and 28.32±16.95 nmol/mg protein (n=27), respectively, versus 4.81±2.64 U/mg protein (n=14) and 14.09±6.66 nmol/mg protein (n=15), respectively, for normal adjacent tissues. The mean arginase activity and ornithine levels in malignant tumor tissues were 16.52±11.02 U/mg protein (n=19) and 35.04±18.21 nmol/mg protein (n=18), respectively, versus 4.87±2.75 U/mg protein (n=17) and 14.27±7.19 nmol/mg protein (n=17), respectively, for normal adjacent tissues. Arginase activity and ornithine level in benignant skin tumors (p<0.05 for arginase and p<0.01 for ornithine) and in malignant skin tumors (p<0.01 for both of them) were found to be higher than those found in adjacent normal tissues.There was also a significant difference between arginase activities of benignant and malignant skin tumors (p<0.05). As a result, we may report that, although arginase activity and ornithine levels are increased in benignant and malignant tumors of the human skin, only arginase activity may be useful for distinguishing patients with malignant skin tumors from those with benignant skin tumors.

P60

ERYTHROCYTE ARGINASE ACTIVITY IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

Selma SÜER GÖKMEN ¹, Reyhan YILDIZ ¹, Fatih ÖZÇELİK ², Zihni AKTAŞ ², Şendoğan GÜLEN ¹

Arginase, the enzyme catalyzing the hydrolysis of arginine to urea and ornithine, is mostly found in the liver. In extrahepatic tissues, arginase is believed to supply the cell with ornithine, a precursor of the polyamines. It has been reported that polyamines are one of the intracellular factors that contribute to isoproterenol-mediated cardiac injury in the rat. It has been suggested that determination of arginase activity in serum may serve as a useful test in early differential diagnosis of myocardial infarction. A crucial point for the clinical utility of a marker is the time from the first investigation of the patient and blood sampling until the time a result is available which is then used for clinical and therapeutic decision making by the phyician. In this setting, we think that determination of arginase activity in erythrocyte instead of serum will offer a more rapid results. The purpose of the present study is to investigate erythrocyte arginase activity in patients with acute myocardial infarction and to evaluate whether it can be used as a biological marker for diagnosis of myocardial infarction. In this study, 58 patients (age 55.46±9.63 years) and 37 healthy volunteers( age 52.24±8.71 years) were included. Arginase activity was determined by the method of Geyer and Dabich. Student’s t-test was used to analyze the results. One unit of arginase was defined as the amount of enzyme that released 1µmol of urea for 1 minute at 37 ⁰C. Arginase activity was found to be 67.17±20.89 U/g hemoglobin in patient group and 51.51±11.36 U/g hemoglobin in control group. Erythrocyte arginase activity at 24h post-infarction in patients with acute myocardial infarction was significantly higher than those found in control group (p<0.001). In conclusion, we may report that there is a significant increase in erythrocyte arginase activity and determination of erythrocyte arginase activity may offer a more rapid result and may be used as a biological marker for diagnosis of patients with acute myocardial infarction.

P61

SERUM TOTAL SIALIC ACID IN PATIENTS WITH BENIGNANT AND MALIGNANT SKIN TUMORS

Selma SÜER GÖKMEN¹, Cemal KAZEZOĞLU¹, Bendigar SUNAR¹, A. Cemal AYGIT², Beyhan ÇAKIR²

Sialic acids, a group of acylated neuraminic acids, are widely distributed in nature as terminal sugars on oligosaccharides attached to protein or lipid moieties. They impart a net negative charge to cell surface and are important in cell-to-cell or cell-to-matrix interactions. Alterations in the metabolism of sialic acid in the presence of malignancy have been reported by some investigators. The aim of the present study is to investigate whether serum total sialic acid can be used as a tumor marker for distinguishing patients with benignant or malignant skin tumors from each other and from healthy subjects. In this study, 36 patients with benignant skin tumors (17 men, age 46.28±16.90 years), 23 patients with malignant skin tumors (15 men, age 49.61±12.60 years) and 36 healthy volunteers (19 men, age 48.47±8.65) were included. Serum total sialic acid determination was performed by the thiobarbituric acid method described by Warren. We compared differences between two patient groups and, between patient and control groups using Student’s t-test.The mean serum total sialic acid levels were found to be 62.30±11.80 mg/dl in patients with benignant skin tumors, 68.31±11.27 mg/dl in patients with malignant skin tumors and 51.40±4.26 mg/dl in control group. There was a significant difference between serum total sialic acid levels of control group and patients with benignant or malignant skin tumors (p<0.001 for both of them). Serum total sialic acid levels of patients with benignant skin tumors was not different from those with malignant skin tumors. In conclusion, we may report that the measurement of serum total sialic acid levels may be useful for distinguishing patients with benignant or malignant skin tumors from healthy subjects, but it cannot be used as a tumor marker for distinguishing patients with benignant skin tumors from those with malignant skin tumors.

P62

SERUM CERULOPLASMIN AND SIALIC ACID LEVELS IN ACUTE MYOCARDIAL INFARCTION

Özgül GÜNGÖR¹, Bendigar SUNAR¹, Fatih ÖZÇELİK², Zihni AKTA޲, Selma SÜER GÖKMEN¹

Sialic acid concentration is increased after myocardial infarction but the reason for this elevation remains obscure. An increased output of acute phase proteins has been reported to be responsible for an elevation in serum total sialic acid (TSA) concentration.The aim of the present study is to investigate serum TSA and ceruloplasmin levels at 24h post-infarction and to evaluate the role of ceruloplasmin, which contains sialic acid residues, in the elevation of sialic acid concentration in myocardial infarction. In this study, 45 patients (male 33) with myocardial infarction and 45 healthy volunteers (male 26) ranging in age from 40 to 70 were included. Serum TSA determination was carried out by the thiobarbituric acid method of Warren and serum aspartate aminotransferase, lactate dehydrogenase and creatine kinase-MB activities and ceruloplasmin levels were measured with an automatic biochemistry analyzer. Student’s t test and Pearson’s correlation test were used to analyze the results. The mean activity of the enzymes in patients group were higher than those found in control group (p<0.001 for all). Serum TSA and ceruloplasmin concentrations were found to be 66.47 ± 9.08 mg/dl and 66.69 ± 8.12 mg/dl in patients , and 53.81 ± 5.74 mg/dl and 30.35 ± 8.20 mg/dl in control group, respectively. Serum TSA (p<0.001) and ceruloplasmin (p<0.001) levels in patients were significantly higher than control group. Patient and control groups were also divided into two age groups: 40-54 years and 55-70 years. Serum TSA and ceruloplasmin levels in 40-54 years and 55-70 years of patients with myocardial infarction were significantly higher when compared with those found in control group (p<0.001 for all). Furthermore, there was a significant difference between the levels of ceruloplasmin in 40-54 years and 55-70 years of control group (p<0.001).There was no correlation between serum TSA and ceruloplasmin levels in patients (r=0.038, p>0.05) and in control group (r= -0.272, p>0.05). As a result, we may report that serum TSA and ceruloplasmin levels are elevated at 24h post-infarction in patients with acute myocardial infarction and an increased output of ceruloplasmin from the liver cannot be only factor responsible for an increased serum TSA concentration following myocardial infarction.

P63

InsulIn-actIvatED GPI-TRANSAMIDASE IN HUMAN erythrocyteS