Yasar Enli

The effects of desferrioxamine on cisplatininduced lipid peroxidation and the activities of antioxidant enzymes in rat kidneys

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and super oxide dismutase (SOD) levels were found to be significantly decreased (P B < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P B < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.

Oxidative stress parameters in patients with slow coronary flow.

IntroductionWe investigated the probable role of free-radical damage in the pathogenesis of slow coronary flow (SCF) by using oxidative stress parameters.MethodsSixty-four patients with angiographically proven SCF and 63 patients with normal coronary flow (NCF) pattern with similar risk profiles were enrolled in this study. We measured erythrocyte superoxide dismutase (SOD), reduced glutathione (GSH), serum malondialdehyde (MDA), catalase and myeloperoxidase (MPO) levels in all subjects.ResultsThere were statistically significant differences in the levels of erythrocyte SOD, GSH and serum MDA between the 2 groups. Serum MDA (P=0.003) and erythrocyte SOD levels (P=0.0001) were increased in the SCF group. The level of erythrocyte GSH (P=0.010) was lower in patients with SCF. There were no differences between the groups’ serum catalase (P=0.682) and MPO levels (P=0.070).ConclusionOur data showed that in patients with SCF, serum MDA and erythrocyte SOD levels were increased while erythrocyte GSH levels were decreased significantly, compared with NCF patients. These results indicate that free-radical damage may play a role in the pathogenesis of SCF.

Carotid intima-media thickness in coronary slow flow: relationship with plasma homocysteine levels.

Background and objectiveCoronary slow-flow phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. Thus, it still remains to be determined whether either microvascular or epicardial diffuse atherosclerotic disease is related to slow flow. In this study, we aimed to determine the carotid artery intima–media thickness, which is a marker of atherosclerosis in patients with coronary slow flow, and its possible relationship with the total homocysteine level. MethodThe study population consisted of 88 patients who underwent coronary angiography because of typical and quasi-typical symptoms of angina. Forty-four patients with angiographically proven coronary slow flow and 44 individuals with normal coronary flow pattern with similar risk profiles were enrolled in the study. Coronary flow patterns of the latter were determined by the thrombolysis in myocardial infarction frame count method. Intima–media thickness was measured by recording ultrasonographic images of both the left and the right common carotid artery with a 12-MHz linear array transducer. Plasma homocysteine, folate and B12 levels were measured from blood samples. ResultsPlasma homocysteine levels (μmol/l) and carotid intima–media thickness (mm) of patients with coronary slow flow were found to be significantly higher than that of controls (12.4±4.9 vs. 8.5±2.8, P=0.0001; 0.75±0.08 vs. 0.69±0.06, P=0.0001, respectively). The plasma folate level (ng/ml) was lower in coronary slow-flow patients than in controls (13.8±4.4 vs. 16.5±5.6, P=0.014). The plasma homocysteine level was significantly positively correlated with the mean thrombolysis in myocardial infarction frame count and intima–media thickness of the carotid artery in correlation analysis (r=0.58, P=0.0001; r=0.41, P=0.0001; respectively). ConclusionHomocysteine levels and carotid intima–media thickness increased but folate levels decreased in patients with coronary slow flow. The present findings allow us to conclude that the possible disturbance in the metabolism of homocysteine in patients with coronary slow flow may have a role in the etiopathogenesis of this phenomenon by causing generalized atherosclerosis.

Elevated Homocysteine Levels in Patients with Slow Coronary Flow: Relationship with Helicobacter pylori Infection

Background and objective:  Elevation of plasma homocysteine (Hcy) level has been implicated in the pathogenesis of slow coronary flow (SCF) as it can severely disturb vascular endothelial function. Helicobacter pylori chronically infect the human stomach and causes malabsorption of vitamin B12 and folate in food, leading ultimately to an increase in circulating Hcy levels.

Effect of Homocysteine-Induced Oxidative Stress on Endothelial Function in Coronary Slow-Flow

Background and Objective: Coronary slow-flow (CSF) phenomenon is characterized by delayed opacification of vessels in a normal coronary angiogram, but its etiopathogenesis remains unclear. Plasma homocysteine (Hcy) level can severely disturb vascular endothelial function and may play a role in the pathogenesis of CSF. In our study, endothelial function in patients with CSF and their relationship with Hcy and oxidative stress parameters are investigated. Method: Forty-four patients with angiographically proven CSF and 44 cases with normal coronary flow pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases are determined by Thrombolysis in Myocardial Infarction (TIMI) frame count method. Endothelium dependent flow mediated dilatation (FMD) and independent vasodilatation characteristics are evaluated by high frequency ultrasound over the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the end product of lipid peroxidation, malondialdehyde (MDA) are measured as oxidative stress markers in blood samples. Results: Plasma Hcy level (µmol/l) of patients with CSF was found to be significantly higher than in controls (12.2 ± 4.9 vs. 8.5 ± 2.8, p = 0.0001). FMD was 7.87 ± 2.0% in controls and 4.98 ± 1.1% in patients with CSF (p = 0.0001). GSH was reduced in patients with CSF. SOD and MDA activity were found higher in patients with CSF than control subjects. Plasma Hcy level was significantly positively correlated with mean TIMI frame count and negatively correlated with FMD in correlation analysis (r = 0.58, p = 0.0001; r = –0.41, p = 0.022; respectively). Conclusion: The present findings allow us to conclude that patients with CSF have increased levels of Hcy and oxidative stress markers and impaired endothelial cell function.

microRNA -143 and -223 in obesity

BACKGROUND Obesity alters endocrine and metabolic functions of adipose tissue and has been recognized as a chronic inflammatory disease, which in turn may contribute to the development of insulin resistance, type 2 diabetes, obesity-associated vasculopathy and cardiovascular disease. The pathogenesis of obesity involves many regulatory pathways including transcriptional regulatory networks, including microRNAs. METHODS A total of 83 patients were included in the study. Patients were recruited from a cardiology outpatient clinic and were allocated into 3 age- and sex-matched groups according to their body mass index. Group 1 included 23 morbidly obese, group 2 30 obese, and group 3 30 normal or overweight subjects. RESULTS In our study, we showed that miR-143 and miR-223 levels were significantly lower in groups 1 and 2 than the control group (normal BMI or overweight). CONCLUSIONS Obesity leads to alterations in miRNA expressions and miRNA-143 and -223s can be used as biomarkers for the metabolic changes in obesity.

Serum Fetuin-A levels, insulin resistance and oxidative stress in women with polycystic ovary syndrome

Abstract This study was designed to determine serum Fetuin-A levels and establish whether serum Fetuin-A level is related with insulin resistance, oxidative stress, ovarian hyperandrogenism and dyslipidemia in women with polycystic ovary syndrome (PCOS). Twenty-two patients with PCOS and twenty-one healthy control women were evaluated in this controlled clinical study. Serum Fetuin-A, lipid fractions, glucose, insulin, malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), superoxide dismutase (SOD) and other hormone (gonadotropins, androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-R). The women with PCOS had significantly higher serum fasting glucose, insulin, luteinizing hormone (LH), MDA, Fetuin-A levels, and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI), HOMA-IR than healthy women. However, sex hormone-binding globulin (SHBG) and GSH levels were significantly lower in patients with PCOS compared with controls. Fetuin-A was positively correlated with insulin, HOMA-IR and FAI. Multiple regression analysis revealed that FAI was strong predictor of serum Fetuin-A level. Serum Fetuin-A level was related with insulin resistance and ovarian hyperandrogenism in women with PCOS. These results suggest that Fetuin-A may have a role in triggering the processes leading to insulin resistance and androgen excess in PCOS.

Interaction of Plasma Homocysteine and Thyroid Hormone Concentrations in the Pathogenesis of the Slow Coronary Flow Phenomenon

Background and Objective: The slow coronary flow (SCF) phenomenon is an angiographic observation and a well-recognized clinical entity characterized by delayed opacification of vessels in a normal coronary angiogram due to reasons yet unclear. Thyroid hormones exert significant effects on plasma homocysteine (Hcy) levels and microvascular resistance. Recently, several investigators have consistently reported that elevation of the plasma Hcy level can severely disturb vascular endothelial function and play a role in the pathogenesis of SCF. Accordingly, we investigated the levels of plasma Hcy and thyroid hormones and their relationship in patients with SCF. Method: Forty-four patients with angiographically proven SCF (Group I) (mean age 55.5 ± 10.4 years, 26 males) and 44 cases with normal coronary flow (NCF) pattern (Group II) (mean age 53.9 ± 11 years, 22 males) with similar risk profiles were enrolled in the study. Coronary flow patterns of the cases were determined by the thrombolysis in myocardial infarction (TIMI) frame count method. The coronary TIMI frame counts were calculated separately for each coronary artery and their average was determined as the mean TIMI frame count for each subject. Serum levels of free tri-iodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH) and Hcy were measured. Patients with thyroid disease or on medications with a potential to affect thyroid functions were excluded. Results: There were no statistically significant differences between the groups concerning the demographic characteristics and major cardiovascular risk factors. Mean TIMI frame counts of SCF and NCF groups were 45.9 ± 12 and 23.3 ± 3.7, respectively. fT4 (ng/dl) and TSH (µIU/ml) levels of the two groups were similar (p > 0.05). The level of fT3, the active metabolite of the thyroid hormone family, was dramatically reduced in the SCF group when compared to the NCF group (2.3 ± 0.2 vs. 3.0 ± 0.3, p = 0.0001, respectively). Plasma Hcy levels of patients with SCF were found to be significantly higher than controls (12.2 ± 4.9 vs. 8.5 ± 2.9, p = 0.0001, respectively). Correlation analysis showed a significant negative correlation between the plasma fT3 and Hcy levels and the mean TIMI frame counts (r = –0.31, p = 0.003 vs. r = –0.66, p = 0.0001). Moreover, there was a significant positive correlation between the plasma Hcy levels and the mean TIMI frame counts (r = 0.58, p = 0.0001). Also, fT3 was the only significant determinant of the variance of Hcy in multiple regression analysis (r = –0.30, p = 0.005). Conclusion: fT3 levels were decreased and plasma Hcy levels were increased significantly in patients with SCF as compared to controls. This finding suggests that thyroid hormones and/or (?) a possible disturbance in their metabolism may be responsible for the elevated levels of plasma Hcy in patients with SCF and may play a role in the pathogenesis of the SCF phenomenon.

Effects of acute exercise on the levels of iron, magnesium, and uric acid in liver and spleen tissues.

In this study, we investigated the effects of acute exercise on tissue levels of iron, magnesium, and uric acid of rats. Twenty adult Wistar albino rats were used for the study. They were divided into two groups: controls (n=10) and the study group (n=10). The study group was left into a small water pool and allowed to do swimming exercise for 30 min while controls rested. All of the animals were sacrificed, and their livers and spleens removed and homogenized immediately. The iron, magnesium, and uric acid levels of the homogenates were measured by an autoanalyzer (ILAB 900, Italy) with commercial kits from the same company. Results were evaluated by the Mann-Whitney U-test. According to our results, the liver iron levels increased significantly with exercise, whereas spleen iron levels decreased significantly (p<0.05) compared to controls. We found no significant differences in the levels of the other two parameters with exercise. These results show that the iron distribution in organs changes with exercise.

Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks

Summary Background Aluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain. Material/Methods We used a chick embryonic development model, with Al treatment of 500 μg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool. Results This Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model. Conclusions Exposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.