The objective of this study was to investigate the effects of trimetazidine (TMZ) on tissue damage in kidney after hindlimb ischemia-reperfusion (I/R), by assessing blood biochemical assay and histopathological analysis. Adult male Wistar rats were divided into two groups. TMZ 10 mg kg −1 day −1 was administrated twice a day for 10 days to the treatment group (group T, n = 10). Sham group was given only 5% gum arabic (group S, n = 10). On 11th day of treatment, 8 h I/R period was performed on right hindlimb of the rats. At the end of reperfusion period, a 5 ml blood withdrawn from ascending aorta for biochemical assays and their right kidneys were harvested for histopathological examination. Superoxide dismutase, Na + -K + ATPase, and reduced glutathione levels were significantly increased in group T (P < 0.001). On the other hand, myeloperoxidase and malondialdehyde levels were significantly less in group T than group S (P < 0.001). Kidneys from the sham-operated group displayed intense leukocytic infiltration in histopathological examination.

Overproduction of reactive oxygen and nitrogen species leads to oxidative stress and decreased total antioxidant capacity, which is responsible for high mortality from several diseases such as endotoxic shock. Nitric oxide (NO) produced by inducible NO synthase (iNOS) during endotoxemia is the major cause of vascular hyporeactivity, hypotension and multiple organ failure. In this study, we investigated whether increased production of NO contributes to renal oxidative stress in endotoxemic rat. Saline (4 mL kg 1 , i.p.), endotoxin (Escherichia coli lipopolysaccharide, O111:B4; 10 mg kg 1 , i.p.) and/or selective iNOS inhibitor (1,3-PBIT; 10 mg kg 1 , i.p.) were administered to conscious male Wistar rats and mean arterial blood pressure was recorded at 1, 2, 3 and 4 hr after injection. Nitrite and malondialdehyde (MDA) levels and myeloperoxidase (MPO) activity were measured in the sera and/or kidney homogenates at the end of the experiments. Administration of endotoxin caused hypotension associated with increased systemic and renal nitrite production. 1,3-PBIT prevented these effects of endotoxin at 1 hr after injection of endotoxin. Renal MPO activity was decreased by endotoxin which was not changed by 1,3-PBIT. Endotoxin caused a decrease in MDA levels in the renal tissue, which was prevented by 1,3-PBIT. These data suggest that overproduction of NO by iNOS during endotoxemia decreases renal oxidative stress and that inhibition of iNOS restores total renal antioxidant capacity.

Glutathione S-transferase (GST) enzymes play an important role in drug metabolism. GST is a multigene family of enzymes involved in the detoxification and in a few instances activation of a wide variety of chemicals. Detoxification features make it plausible to search for GST polymorphism in patients with drug eruption. The GSTM (mu), GSTT (theta) and GSTP (pi) have been shown to be polymorphically distributed. The GSTT1, GSTM1 and GSTP1 gene polymorphism were detected using real-time PCR. GSTM1 and GSTT1 null genotypes were found to be associated with an increased risk of drug eruption (OR 2.27, 95% CI 1.20–5.21; OR 2.48, 95% CI 1.12–6.39, respectively). No relationship was observed between the null combination of the GSTM1 and GSTT1 genotype polymorphisms and drug eruption risk (OR 2.65, 95% CI 0.62–11.25). Our results show that GSTP1 polymorphism is not a significant contributor to drug eruption risk. The GSTM1 and GSTT1 gene polymorphisms seem to be associated with the development of drug eruption. Further studies may shed additional light on the role of GSTM1, GSTT1 and GSTP1 in drug eruption.

Purpose To investigate the role of oxidative stress and lipid peroxidation in the pathogenesis of primary open-angle glaucoma (POAG). Materials and methods The activities of myeloperoxidase (MPO), catalase (CAT), and the levels of plasma malondialdehyde (MDA) were measured in 40 (15 men and 25 women) patients with POAG and 60 (30 men and 30 women) healthy controls.

Purpose Oxidative mechanisms play a major role in the aetiology and pathogenesis of cataract, especially in age-related cataract. Our study aims to investigate systemic oxidant and antioxidant markers in cataract patients. Methods The activity of erythrocyte catalase and the level of malondialdehyde in plasma were measured in 40 patients with cataract and 60 healthy control subjects. The malondialdehyde level, as an index of lipid peroxidation, was determined by thiobarbitü ric acid reaction according to Yagi.

We examined whether nitric oxide (NO), derived from constitutive NO synthase (NOS) and/or inducible NOS (iNOS), could contribute to endotoxin-induced inflammatory hyperalgesia via interacting with nuclear factor-B (NF-B), inducible cyclooxygenase (COX-2) and/or polyADPribose synthase (PARS). Injection of endotoxin (10 mg kg −1 , i.p.) to mice elicited hyperalgesia, determined by hot plate test, which is prevented by NO precursor (l-arginine), cNOS/iNOS inhibitor (N G -nitro-l-arginine methyl ester; l-NAME), NF-B inhibitor (N-acetylserotonin), COX inhibitor (indomethacin), COX-2 inhibitor (DFU) and PARS inhibitor (3-aminobenzamide). Endotoxin caused a decrease in serum nitrite levels prevented by N-acetylserotonin, l-arginine, indomethacin, DFU or 3-aminobenzamide. Endotoxin increased serum 6-keto-PGF 1␣ levels diminished by l-arginine or aminoguanidine (iNOS inhibitor). l-Arginine, l-NAME, aminoguanidine, DFU or 3-aminobenzamide prevented endotoxin-induced decrease in heart, lungs, kidneys and brain nitrite and malonedialdehyde levels and myeloperoxidase activity. In conclusion, NO reverses endotoxin-induced inflammatory hyperalgesia via inhibition of prostacyclin production, and also contributes to the analgesic effect of NF-B, COX or PARS inhibitors.

Background Recent studies have suggested that there might be an etiologic role for Helicobacter pylori (HP) in rosacea. HP is a Gram-negative bacterium that colonizes the gastric mucosa, increases the generation of reactive oxygen species (ROS), and decreases plasma antioxidants such as ascorbic acid.

Background Recent studies have suggested that there might be an etiologic role for Helicobacter pylori (HP) in rosacea. HP is a Gram-negative bacterium that colonizes the gastric mucosa, increases the generation of reactive oxygen species (ROS), and decreases plasma antioxidants such as ascorbic acid.

Letters for both). After a single dilating session, excel lent results were obtained in 31 patients (70.5%), good results in five (11.4%), fair in five (11.4%), and poor results in three (6.8%) patients. Pneu matic dilation was successful in 36/44 (81.8%) patients after a single session and in 38/44 (86.4%) patients overall. There were no serious complica tions or mortality.

Protective role of selenium against free radical damage was first demonstrated in the heart and this effect was further questioned in other systems. In the present study, the effects of exogenously administered selenium on intestinal fine morphology, lipid peroxidation, and bacterial translocation (BT) in experimental intestinal ischemia/reperfusion (I/R) model were examined. Thirty-two male Wistar rats weighing 250-300 g were randomized into four groups. Sham group (n = 8) underwent laparotomy only. In the I/R group (n = 8), laparotomy was performed and the superior mesenteric artery was occluded using an atraumatic microvascular clamp for 30 min. In corresponding selenium-treated groups (n = 8 each), sodium selenate was given 0.2 mg kg −1 day −1 intraperitoneally (i.p.) for 3 consecutive days, prior to surgery for either laparotomy only or with I/R. Twenty-four hours later, tissue samples from liver, spleen, and mesenteric lymph nodes were obtained under sterile conditions for microbiological analysis and further evaluation of I/R-induced intestinal injury. Ileum samples were fixed in 10% formaldehyde for histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, and liver was significantly higher than other groups (P < 0.05). Selenium supplementation prevented I/R-induced BT and significantly reduced the I/R-induced intestinal injury (P < 0.05). Tissue MDA levels from the ileum specimens of selenium-treated rats were significantly lower than that of the I/R group (P < 0.05). Our results provide evidence that the relationship between BT and lipid peroxidation in intestinal tissue is crucial. Selenium pretreatment reduces lipid peroxidation which contributes to the maintenance of intestinal mucosal integrity.

Although the precise mechanism by which sepsis causes impairment of respiratory muscle contractility has not been fully elucidated, oxygen-derived free radicals are thought to play an important role. In our experimental study, the effects of poly(ADP-ribose) synthetase (PARS) inhibition on the diaphragmatic Ca 2+ -ATPase, malondialdehyde (MDA), and 3-nitrotyrosine (3-NT) levels and additionally histopathology of the diaphragm in lipopolysaccharide (LPS)-induced endotoxemia are investigated.

Coronary artery disease (CAD) is the leading cause of morbidity and mortality in the world, and cigarette smoking is a major contributing factor to the disease. Glutathione S-transferase (GST) enzyme is implicated in the detoxification of carcinogens present in tobacco smoke and consequent polymorphisms in this gene may confer susceptibility to cardiovascular disease if DNA damage is important in CAD. Therefore, we examined this question in a case-control study of subjects having coronary atheroma by angiography and with a past history of myocardial infarction (MI). The study population consists of 247 healthy controls and 148 consecutive patients who had undergone coronary angiography for suspicion of coronary artery disease. DNA was extracted from whole blood, and the GSTM1 and GSTT1 polymorphisms were determined using a real-time polymerase chain reaction (PCR). We found that the null GSTM1 and GSTT1 genotypes were associated with an increase in the risk of developing coronary heart disease (OR = 1.14; 95% CI: 0.71 – 1.82; OR = 1.38; 95% CI: 0.82 – 2.32), respectively, but this increase was not significant. Patients who smoke having the null genotypes of GSTM1 (OR: 1.63 (1.10 – 2.63)) and GSTT1 (2.66 (1.50 – 4.72)) and both (3.20 (1.37 – 7.45)) were at a higher risk for developing coronary heart disease. In conclusion, the finding of a significant association between GSTM1 and T1 with smoking status may influence cardiovascular disease via DNA damage.