Homocysteine and nitric oxide in patients undergoing diagnostic coronary angiography.

We evaluated the plasma homocysteine (tHcy) and nitric oxide metabolites (nitrite plus nitrate; NOx) data of consecutive patients undergoing diagnostic coronary angiography (n=79) with respect to the presence and severity of coronary artery disease (CAD), the presence of acute coronary syndromes (ACS), and the risk status of patients. Hyperhomocysteinemia (&#62;15 micromol/L) was detected in 11% of the controls (n=19) and 37% of CAD patients (n=60) (p=0.03). Plasma tHcy in CAD patients was not significantly different from controls, but those with 3-vessel disease had a significantly higher tHcy concentrations than did controls (p=0.049). The patients with 3-vessel disease and ACS had the highest concentrations of tHcy (16.9 +- 4.4 micromol/L), and the difference from the ACS patients with 1- and 2-vessel involvement was significant (p=0.03). In patients with 1-vessel involvement, tHcy was correlated with NOx (r=0.62, p=0.005); in patients with 2- and 3-vessel disease this correlation could not be observed. The high-risk patients (n=51) had a higher mean number of vessel involvement and tHcy (p&#60;0.001, p&#60;0.05, respectively) but lower NOx (p&#60;0.05) when compared to the low-risk patients (n=28). It appears that in the early stages of atherosclerosis hyperhomocysteinemia causes an increase in NOx production, but with progression of the disease this compensatory increase disappears.</p

A novel approach for preventing esophageal stricture formation: olmesartan prevented apoptosis

Accidentally ingested corrosive substances can cause functional and structural damage to the esophageal tissue resulting in stricture formation. It has been reported that the administration of olmesartan (OLM) can have anti-inflammatory, antifibrotic and antiapoptotic effects on injured tissue. The aim of our study was to check if OLM could prevent formation of scars in the corrosive esophageal burn model. Fifty-one Wistar Albino rats were divided into six groups: Control, Sham, OLM, Sham + OLM, Burn, and Burn + OLM. Olmesartan (5 mg/kg) was given by gavage once per day for 21 consecutive days after injury. The morphology of the esophagus was assessed after Masson trichrome staining, and apoptosis was evaluated using the terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) method. The serum nucleosomes (as an indicator of apoptosis), serum p53 protein, and esophageal tissue p53 protein levels of each group were measured by immunoassays. Muscularis mucosa damage, submucosal collagen deposition, and tunica muscularis injury in the Burn + OLM group decreased significantly compared with the Burn group (p &lt; 0.05). Similarly, the number of apoptotic cells in the Burn + OLM group decreased compared with the Burn group (p &lt; 0.05). Serum levels of nucleosomes and p53 and tissue of p53 protein did not differ between the groups. Exogenously administered OLM can effectively prevent the occurrence of esophageal strictures caused by corrosive esophageal burns. (Folia Histochemica et Cytobiologica 2014, Vol. 52, No. 1, 29–35

Maternal serum preptin levels in the pathogenesis and diagnosis of Gestational diabetes mellitus

Background: Gestational diabetes mellitus (GDM) is a metabolic disorder that occurs during pregnancy that increases both maternal and fetal mortality and morbidity. It was investigated whether there is a change in circulating levels of preptin, a new peptide secreted from pancreatic beta cells, due to GDM in pregnant women. The relationship between serum preptin levels with insulin and other metabolic parameters was also evaluated in these subjects. Methods: Eighty-five patients diagnosed as GDM and 89 healthy pregnant women with 75 mg oral glucose tolerance test (OGTT) was assessed in terms of serum preptin levels. Results: The serum preptin levels of the GDM group were significantly higher than those of the control group (p=0.001; p < 0.01). For the cutoff value of preptin measurement of 335.3 ng/L, the sensitivity was 97.65%, specificity was 87.64%, positive predictive value was 88.3% and negative predictive value was 97.5%. The risk of developing the disease is 294.273 times higher in patients with preptin level of 335.3 and above. Conclusions: We think that the reason for the increase in serum preptin levels in GDM is probably the response to glucose. The current results indicate that preptin plays an important role in elucidating the pathology of GDM. In addition, the search for a practical marker for the diagnosis of GDM suggests that the measurement of preptin level is promising

Oxidative stress parameters and inflammatory and immune mediators as markers of the severity of sepsis

Introduction: Sepsis is a complex inflammatory syndrome with diverse etiology and wide spectrum of severity. The aim of this study was to investigate whether inflammatory mediators, in comparison with oxidative parameters, are associated with severity of sepsis. Methodology: Plasma neopterin, adenosine deaminase (ADA), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), interleukin (IL)-1, IL-6, and tumor necrosis factor alpha (TNF-alpha), as inflammatory mediators, and serum nitric oxide (NOx), nitrotyrosine (NT), oxidized LDL (oxLDL) levels, serum paraoxonase 1 (PON1) activity, and erythrocyte glutathione (GSH) levels as oxidative stress parameters of 12 patients with mild sepsis, 25 patients with severe sepsis, and 20 healthy control subjects were evaluated. NOx, GSH levels and PON1 activity were determined by colorimetric methods, whereas neopterin, VCAM, ICAM, IL-1, IL-6, TNF-alpha, NT, and oxLDL levels were measured by enzyme-linked immunosorbent assay (ELISA)

Evaluation of oxidative stress markers in first trimester for assessment of preeclampsia risk

The aim of this study is to determine the predictive values of oxidative stress markers and antioxidants in the development of preeclampsia between 10-14 and also at 20-24 weeks of gestation, after the completion of vascular transformation

Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients

Influence of propylthiouracil treatment on oxidative stress and nitric oxide in Basedow disease patients

Oxidative stress parameters and nitric oxide (NO) values were determined in 27 newly diagnosed Basedow patients before and afer 1 mo of propylthiouracil (PTU) therapy and in 15 healthy controls. Basedow patients exhibited increased triiodothyronine (T-3) and thyroxine (T-4) and decreased thyroid-stimulating hormone (TSH) values compared to controls. Significantly higher thiobarbituric acid-reactive substances (TBARS), NO and glutathione (GSH) levels, and CuZn superoxide dismutase (CuZn SOD) activity were found in Basedow patients in comparison to controls, regardless of sex. Treatment with PTU (3 x 100 mg/d for 30 d) was effective in decreasing T-3 and T-4 and increasing TSH levels. Significantly decreased NO and TBARS and increased GSH and CuZn SOD levels were observed in PTU-treated Basedow patients compared to pre-PTU administration. PTU-treated patients compared to controls still exhibited significantly higher T-3 and lower TSH values and higher NO, TBARS, GSH, and CuZn SOD levels. The induced antioxidant defense and decrease in NO values in response to PTU therapy emphasizes the role of PTU as an antithyroid drug, where the ability to diminish hyperthyroidism results in decreased catabolism and lower oxidant generation

Oxidative stress parameters and inflammatory and immune mediators as markers of the severity of sepsis

Introduction: Sepsis is a complex inflammatory syndrome with diverse etiology and wide spectrum of severity. The aim of this study was to investigate whether inflammatory mediators, in comparison with oxidative parameters, are associated with severity of sepsis. Methodology: Plasma neopterin, adenosine deaminase (ADA), vascular cell adhesion molecule (VCAM), intracellular adhesion molecule (ICAM), interleukin (IL)-1, IL-6, and tumor necrosis factor alpha (TNF-alpha), as inflammatory mediators, and serum nitric oxide (NOx), nitrotyrosine (NT), oxidized LDL (oxLDL) levels, serum paraoxonase 1 (PON1) activity, and erythrocyte glutathione (GSH) levels as oxidative stress parameters of 12 patients with mild sepsis, 25 patients with severe sepsis, and 20 healthy control subjects were evaluated. NOx, GSH levels and PON1 activity were determined by colorimetric methods, whereas neopterin, VCAM, ICAM, IL-1, IL-6, TNF-alpha, NT, and oxLDL levels were measured by enzyme-linked immunosorbent assay (ELISA)

The effects of atorvastatin on oxidative stress in L-NAME-treated rats

Objectives. Current evidence suggests that the beneficial vascular effects of statins are not limited to the statins' lipid-lowering properties; these drugs can also improve vascular endothelial cell function. N omega-nitro-l-arginine methyl ester (L-NAME) is a potent synthetic nitric oxide inhibitor, and long-term oral L-NAME treatment is used to induce vascular lesions in experimental animal models. Methods. We determined the effects of statins on protein carbonyl (PCO), lipid hydroperoxides (LHP), oxidized low-density lipoproteins (ox-LDL) and antioxidants such as paraoxonase 1 (PON1) and total thiols (T-SH) in long-term L-NAME-treated rats. Adult male Wistar rats were divided into three groups, namely, control, L-NAME-treated (1 mg/mL in drinking water for three weeks), and atorvastatin plus L-NAME-treated (4 mg/kg/day atorvastatin for 1 week during the third week of L-NAME treatment) groups. Results. In the L-NAME group, the ox-LDL, LHP and PCO were higher and the PON1 and T-SH were lower than the concentrations observed for the controls. When compared with the L-NAME group, the L-NAME plus atorvastatin group had significantly lower ox-LDL and LHP and higher PON1 activities. Additionally, the elevated total cholesterol (TC) and low-density lipoprotein-C (LDL-C) in the L-NAME group were decreased by atorvastatin administration. TC and LDL-C were positively correlated with ox-LDL and LHP and negatively correlated with PON1 in all groups. High-density lipoprotein-C (HDL-C) was negatively correlated with ox-LDL. Conclusion. PON1 prevents LDL oxidation and inactivates LDL-derived oxidized phospholipids; its activity showed a pronounced decrease in the L-NAME treatment group and was increased in the atorvastatin group. Based on our findings, we concluded that the atorvastatin had HDL-related antioxidant activity as well as lipid-lowering properties