Effect of air bubble on inflammation after cataract surgery in rabbit eyes.

PURPOSE: Intense inflammation after cataract surgery can cause cystoid macular edema, posterior synechia and posterior capsule opacification. This experimental study was performed to investigate the effect of air bubble on inflammation when given to anterior chamber of rabbit eyes after cataract surgery. MATERIALS AND METHODS: 30 eyes of 15 rabbits were enrolled in the study. One of the two eyes was in the study group and the other eye was in the control group. After surgery air bubble was given to the anterior chamber of the study group eye and balanced salt solution (BSS; Alcon) was left in the anterior chamber of control eye. RESULTS: On the first, second, fourth and fifth days, anterior chamber inflammations of the eyes were examined by biomicroscopy. On the sixth day anterior chamber fluid samples were taken for evaluation of nitric oxide levels as an inflammation marker. When the two groups were compared, in the air bubble group there was statistically less inflammation was seen. (1, 2, 4. days P = 0,001, and 5. day P = 0,009). CONCLUSIONS: These results have shown that when air bubble is left in anterior chamber of rabbits' eyes after cataract surgery, it reduced inflammation. We believe that, air bubble in the anterior chamber may be more beneficial in the cataract surgery of especially pediatric age group, uveitis patients and diabetics where we see higher inflammation. However, greater and long termed experimental and clinical studies are necessary for more accurate findings.

Effect of clopidogrel on nitric oxide levels in an ischemia reperfusion model.

Ischemia and reperfusion injury is a pathologic process with serious consequences, arising due to interruption of arterial blood flow. Restored blood flow achieved after the ischemic period causes formation of oxygen radicals by activation of a variety of substances and systems. In this study, we investigated the effect of clopidogrel, an antithrombocyte agent, on tissue nitric oxide (NO) levels in an experimental ischemia reperfusion model. For this purpose, 6 hours of ischemia and 4 hours of subsequent reperfusion were applied to the right lower extremities of the subjects. Clopidogrel therapy was started in one of these groups 10 days before the process (study group). NO levels were measured in all groups in the muscle, lung, and liver tissues, and in plasma. Lung, plasma, and liver NO measurement values had statistically significant differences among the groups. There was no statistically significant difference in the measurements made on the muscle tissue. Clopidogrel, which has previously been reported to be suitable to be used as a preventive agent of ischemia reperfusion damage, has had a reducing effect on the NO levels in tissues in the ischemia reperfusion model created in our present study.

Effects of erdosteine on bleomycin-induced lung fibrosis in rats.

This study was designed to examine the effects of erdosteine on bleomycin (BLM)-induced lung fibrosis in rats. Thirty-three Sprague-Dawley rats were divided randomly into three groups, bleomycin alone (BLM), bleomycin + erdosteine (BLM + ERD), and saline alone (control). The BLM and BLM + ERD groups, were given 2.5 mg/kg BLM intratracheally. The first dose of oral erdosteine (10 mg/kg/day) in the BLM + ERD group was started 2 days before BLM administration and continued until animals were sacrificed. Animals were sacrificed 14 days after intratracheal instillation of BLM. The effect of erdosteine on pulmonary fibrosis was studied by analysis of bronchoalveolar lavage (BAL) fluid, histopathology, and biochemical measurements of lung tissue superoxide dismutase (SOD) and glutathione (GSH) as antioxidants, malondialdehyde (MDA) as an index for lipid peroxidation, and nitrite/nitrate levels. Bleomycin-induced lung fibrosis as determined by lung histology was prevented with erdosteine (grades of fibrosis were 4.9, 2.3, and 0.2 in BLM, BLM + ERD, and control groups, respectively). Erdosteine also prevented bleomycin-induced increase in MDA (MDA levels were 0.50 +/- 0.15, 0.11 +/- 0.02, and 0.087+/- 0.03 nmol/mg protein in BLM, BLM + ERD, and control groups, respectively) and nitrite/nitrate (nitrite/nitrate levels were 0.92 +/- 0.06, 0.60 +/- 0.09, and 0.56+/- 0.1 micromol/mg protein in BLM, BLM + ERD, and control groups respectively) levels. Bleomycin-induced decrease in GSH and SOD levels in the lung tissue also prevented by erdosteine [(GSH levels were 213.5 +/- 12.4, 253.2+/- 25.2, and 287.9+/- 34.4 nmol/mg protein) (SOD levels were 1.42+/- 0.12, 1.75+/- 0.17, and 1.89+/- 0.09 U/mg protein) in BLM, BLM + ERD, and control groups respectively]. Erdosteine prevented bleomycin-induced increases in total cell number and neutrophil content of the BAL fluid. In conclusion, oral erdosteine is effective in prevention of BLM-induced lung fibrosis in rats possibly via the repression of neutrophil accumulation, inhibition of lipid peroxidation, and maintenance of antioxidant and free radical scavenger properties.

Protective effects of N-acetylcysteine on the peroxidative changes of rat lungs exposed to inhalation of thinners.

OBJECTIVE: Long-term inhalation of thinners may cause damage, both to the lungs and to other organ systems. It causes cellular damage via formation of reactive oxygen species. The lung is protected from oxidative stress by the glutathione (GSH) antioxidant system which can be augmented by the thiol drug, N-acetylcysteine (NAC). This study investigated the protective effect of NAC on peroxidative changes in rat lungs exposed to inhalation of thinners for 8 weeks. METHODOLOGY: Seventy-two male Wistar albino rats were used and divided into two groups: one group inhaled only thinners (TI), while the other inhaled TI plus NAC. Rats in the TI and TI + NAC groups were divided into four subgroups (each consisting of eight rats) according to the duration of exposure to TI: 2, 4, 6 and 8 weeks. A control group (n = 7) of rats inhaled neither TI nor NAC. Malondialdehyde (MDA) and GSH levels, and superoxide dismutase (SOD) activities were determined in the lung tissues. Histopathological findings were evaluated as acute and chronic changes in the alveoli and interstitium in the TI and TI + NAC groups and compared with those in the control group. RESULTS: While tissue MDA levels in the groups inhaling TI for 4, 6 and 8 weeks were significantly higher than those in the control groups (P < 0.01, P < 0.01, P < 0.0001, respectively), GSH levels were significantly lower (P < 0.05, P < 0.01, P < 0.01, respectively). Tissue SOD activities in the groups inhaling TI for 6 and 8 weeks were significantly lower than those in the control group (P < 0.05, P < 0.01, respectively). In the TI group, MDA levels were significantly increased (P < 0.01) with increasing duration of inhalation (from the second week through to the eighth week), while GSH levels and SOD activities were significantly decreased (P < 0.01, P < 0.01). Tissue MDA levels were significantly lower in the TI + NAC groups across all inhalation periods, when compared with the TI groups (P < 0.01, P < 0.0001, P < 0.0001, P < 0.0001, respectively). Tissue GSH levels in the TI + NAC groups were significantly higher than those of the TI groups (respective values: P < 0.05, P < 0.01, P < 0.01, P < 0.0001). Tissue SOD activities in the TI + NAC groups were significantly higher than those of the TI groups (respective values: P < 0.05, P < 0.0001, P < 0.05, P < 0.0001). Pathological examinations with light microscopy did not show any beneficial effect of NAC application in terms of deferring or alleviating the negative effects of TI. CONCLUSIONS: Thinners are agents that cause imbalance between oxidants and antioxidants produced by aerobic cellular systems. This imbalance between oxidant and antioxidant systems is decreased by the effect of NAC. However, ultrastructural studies may be needed to substantiate this evidence morphologically, as light microscopy was inconclusive.

Malondialdehyde, glutathione, glutathione peroxidase and homocysteine levels in type 2 diabetic patients with and without microalbuminuria.

BACKGROUND: High levels of homocysteine and oxidative stress are known to be associated with premature vascular disease in type 2 diabetes mellitus (DM). The aim of this study was to estimate homocysteine levels and oxidant-antioxidant status and to determine the relationship between them in type 2 diabetic patients with and without microalbuminuria. METHODS: Fasting blood samples were obtained from 48 diabetic patients (17 with and 31 without microalbuminuria) and 20 healthy subjects. Serum total homocysteine (tHcy), plasma malondialdehyde (MDA) erythrocyte glutathione (GSH) and glutathione peroxidase (GPx) activity were measured in these patients and the results were compared with those of controls who were chosen among healthy subjects. RESULTS: MDA levels were found to be significantly lower and GSH levels and GPx activities were found to be significantly higher in control subjects when compared with patients with and without microalbuminuria (MDA: P < 0.0001, P < 0.0001; GSH: P < 0.0001, P < 0.0001; GPx: P < 0.0001, P < 0.001, respectively). MDA levels were found to be significantly higher in patients with microalbuminuria compared with patients without microalbuminuria (P < 0.0001), while similarly GSH levels were found to be significantly lower in patients with microalbuminuria (P < 0.0001). Although there were no significant differences with respect to tHcy levels and GPx activities between the microalbuminuric and normoalbuminuric patients (P > 0.05), there was a significant difference with respect to tHcy levels between healthy controls and patients with microalbuminuria (P < 0.05). The serum levels of tHcy correlated best with plasma MDA and erythrocyte GSH concentrations in all diabetic patients (r = 0.549, P < 0.0001; r = -0.385, P<0.01). CONCLUSION: Decreased antioxidant levels, increased lipid peroxidation and increased tHcy levels were observed in patients with microalbuminuria. These changes may contribute to vascular disease, which is particularly prevalent in type 2 DM patients with microalbuminuria.

Homocysteine and nitric oxide levels in plasma of patients with pseudoexfoliation syndrome, pseudoexfoliation glaucoma, and primary open-angle glaucoma.

PURPOSE: To evaluate plasma total homocysteine (tHcy) and nitric oxide (NO) marker levels in patients with pseudoexfoliation syndrome (PXS), pseudoexfoliation glaucoma (PXG), primary open-angle glaucoma (POAG), and normal controls. METHODS: This cross-sectional, prospective study involved 19 patients with POAG, 18 with PXS, 22 with PXG, and 20 control subjects. Fasting tHcy levels of all study participants were determined using a fluorescence polarization immunoassay method. Quantitation of total nitrate was based on the Griess reaction, in which a chromophore with a strong absorbance at 545 nm is formed by reaction of nitrite with a mixture of naphthylethylenediamine and sulphanilamide. RESULTS: The mean plasma homocysteine level was statistically significantly elevated in the PXS (p=0.033) and the PXG (p=0.023) groups but not in the POAG group (p=0.996) when compared with the control group. Multiple logistic regression analyses comparing the various patient groups with the single control group indicated that elevation in plasma homocysteine concentration was a significant risk factor for PXS (odds ratio per 1 micromol/l increase in homocysteine concentration=2.05, 95% CI=1.19-3.52) and PXG (odds ratio per 1 micromol/l increase in homocysteine concentration=1.36, 95% CI=1.00-1.85) but was not a significant risk factor for POAG (odds ratio per 1 micromol/l increase in homocysteine concentration=0.99, 95% CI=0.78-1.26). NO markers levels were found to be slightly higher in PXS and PXG patients than control and POAG patients but the differences were not statistically significant (p=0.151). Multiple logistic regression analyses comparing the various patient groups with the single control group indicated that elevation in NO marker concentration was not a significant risk factor for PXS (odds ratio per 1 micromol/l increase in NO concentration=1.00, 95% CI=0.99-1.01), PXG (odds ratio per 1 micromol/l increase in NO concentration=1.00, 95% CI=0.99-1.00) and POAG (odds ratio per 1 micromol/l increase in NO concentration=0.99, 95% CI=0.99-1.00). No statistically significant correlations were observed between plasma tHcy and NO markers in study groups (p>0.05). CONCLUSION: Elevated levels of homocysteine in pseudoexfoliation patients with and without glaucoma may partly explain the increased risk of vascular disease among patients with pseudoexfoliation. No significant difference was found in plasma NO markers among the POAG, PXS, PXG, and the control subjects.

Protective effects of clopidogrel on oxidant damage in a rat model of acute ischemia.

Reperfusion injury is a consequence of inadequate energy supply and acidosis in ischemic tissues and a chain of events triggered by oxygen-derived free radicals released in response to exposure of oxygen. In this study, we aimed to assess the effects of clopidogrel, an antithrombotic agent, on experimental ischemia-reperfusion model in rats. The ischemia was performed by blockade of the circulation of right lower extremity at trochanter major level for 6 hours. Then, the extremity was reperfused for 4 hours. Another group of rats pretreated with clopidogrel (0.2 mg/kg/day) for 10 days prior to ischemia-reperfusion. After the reperfusion period, all rats were anesthetized with ketamine. Blood and tissue samples from the gastrocnemius muscle, liver and lungs were taken for the measurement of malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) activity. The results revealed that clopidogrel prevented the increase in MDA level and the decrease in GSH level and SOD activity caused by ischemia-reperfusion both in tissue samples and plasma. These findings suggest that clopidogrel is beneficial in prevention of ischemia-reperfusion injury probably via its effects on inflammatory cells, platelets, and endothelial cells.

The effects of thinner inhalation on superoxide dismutase activities, malondialdehyde and glutathione levels in rat lungs.

BACKGROUND: Recent years' usage of thinner by the young generation as a drug constitutes a serious problem in the society. Due to common usage in the industrial sector, most people are affected from the manufacturing process to the consuming phase. AIM: Because of these reasons, this project has been preferred to research the effects of thinner on oxidant and antioxidant status. METHODS: Totally 46 rats were included in the study. Thirty six rats were separated into six groups with 10 rats in a control group. The first group inhaled thinner for 2 weeks, and the other groups were exposed to thinner for 4, 6, 8, 10 and 12 weeks for 1 h twice a day. On the mentioned duration, rats were autopsied. Lung tissues malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) activities were determined to designate the oxidant-antioxidant balance. RESULTS: We observed an increase in MDA values both in the acute and the subacute periods. In the chronic period by the consuming of lipid peroxidation products, MDA values decreased and as the oxidative stress continued MDA values again increased. We observed that especially GSH values that has antioxidant feature, decreased until 6 weeks in order to compensate lipid peroxidation products. In the consuming period of lipid peroxidation, the values became fixed and later, these values again increased. There was no relationship between the changing values of MDA and SOD. CONCLUSIONS: Thinner is an agent that causes oxidative stress and inhalation of high doses of thinner causes harm to the respiratory system. As there are few reports in the literature on long-term effects of thinner inhalation, more studies might be necessary.

The effects of antioxidants on exercise-induced lipid peroxidation in patients with COPD.

OBJECTIVE: The oxidant-antioxidant balance plays an important role in the pathogenesis of COPD. The aim of the present study was to evaluate the effects of exercise, as an oxidative stress factor on the oxidant-antioxidant balance and to investigate whether short-term antioxidant treatment affects lipid peroxidation products. METHODOLOGY: Twenty-one stable COPD patients and 10 control subjects were included in the study. Symptom-limited exercise tests were performed by all subjects. Blood was collected before and 1 h after exercise in control subjects and before, 1 and 3 h after exercise in COPD patients, for analysis of malondialdehyde (MDA), reduced glutathione (GSH) and vitamin E (VE) levels. VE and vitamin C treatments were added to the regular bronchodilator therapy in 10 COPD patients for 1 month. After the treatment period, an exercise test was performed and blood was collected again for MDA, GSH and VE levels. RESULTS: Baseline GSH and VE levels were significantly lower in the COPD group when compared with the control subjects. There was no statistically significant difference in MDA levels between the two groups. In the COPD group, MDA levels 3 h after exercise were significantly higher than at baseline. In contrast there were no significant differences in MDA, VE and GSH levels in the control group after exercise. VE and MDA levels increased significantly after exercise in COPD patients but there was no difference in GSH levels. Baseline exercise time was significantly lower in the COPD group than in the controls. In 10 COPD patients who were given antioxidant therapy, their exercise time increased significantly and there was no increase in MDA and VE levels after the repeated exercise test. CONCLUSIONS: Antioxidant levels were significantly lower in COPD patients than in control subjects. In these patients, exercise results in more significant oxidative stress and lipid peroxidation than in control subjects and antioxidant therapy may decrease lipid peroxidation following exercise and improve exercise capacity.

Plasma lipid and lipoprotein concentrations in pregnancy induced hypertension.

OBJECTIVES: Aim of this study was to evaluate implication of pregnancy induced hypertension on maternal plasma lipid, lipoprotein, apolipoprotein concentrations and lipid peroxidation products by a comparison of normal pregnancy vs. preeclampsia. DESIGN AND METHODS: Thirty-four women with preeclampsia and 32 healthy pregnant women (controls) in the third trimester were recruited for this study. RESULTS: In the preeclamptic group plasma total triglyceride, low density lipoprotein cholesterol (LDL-C), malondialdehyde (MDA) and apolipoprotein B (apo-B) were significantly increased, while plasma high density lipoprotein cholesterol (HDL-C) was significantly decreased compared to that of control group. There was no significant difference in total cholesterol and apolipoprotein A1 (apo-A1) concentrations. CONCLUSION: Our findings suggest that preeclampsia share some metabolic characteristics with coronary artery disease such as dislipidemia and increased lipid peroxidation. However lipoprotein concentrations may be better biochemical markers of dislipidemia in the preeclamptic state than the corresponding apolipoproteins.

Erythrocyte glutathione peroxidase activity, plasma malondialdehyde and erythrocyte glutathione levels in hemodialysis and CAPD patients.

OBJECTIVES: Cardiovascular disease is the major cause of mortality in patients receiving hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) due to chronic renal failure. Increased lipid peroxidation and depletion of antioxidants may contribute to increased risk of atherosclerosis. We have therefore assessed the effect of hemodialysis and CAPD on oxidant and antioxidant status. DESIGN AND METHODS: Plasma malondialdehyde (MDA), Glutathione (GSH) levels and glutathione peroxidase (Gpx) activities were determined in 20 healthy persons (control), 20 patients on HD, 16 patients on CAPD. RESULTS: MDA was elevated in posthemodialysis and CAPD patients in comparison to prehemodialysis and control groups (posthemodialysis 1.39 +/- 0.38 nmol/mL, CAPD 1.26 +/- 0.27 nmol/mL, prehemodilaysis 0.83 +/- 0.22 nmol/mL, controls 0.72 +/- 0.21 nmol/mL p < 0.0001). With respect to antioxidants, glutathione levels were significantly lower in prehemodialysis, posthemodialysis and CAPD groups than those in control group (prehemodialysis 16.82 +/- 6.73 mg/dL RBC, posthemodialysis 31.43 +/- 11.88 mg/dL RBC, CAPD 40 +/- 12.72 mg/dL RBC, controls 62.26 +/- 24.01 mg/dL RBC, p < 0.0001). While erythrocyte GSH levels were significantly lower in the prehemodialysis patients than those in posthemodialysis and CAPD patients (p < 0.0001), it was significantly lower in posthemodialysis patients than those in CAPD patients (p < 0.05). There were no significant differences with respect to erythrocyte Gpx levels among the groups (p > 0.05). CONCLUSIONS: These findings indicate oxidative stress in patients with chronic renal failure which is further exacerbated by hemodialysis and CAPD, as evidenced by increased lipid peroxidation and low antioxidant levels.