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Mustafa Serteser

Publications and source records attributed to Mustafa Serteser.

25 records · Page 2Linked to original sources

Changes in hepatic TNF-alpha levels, antioxidant status, and oxidation products after renal ischemia/reperfusion injury in mice.

BACKGROUND: Ischemia/reperfusion (I/R) injury induces an inflammatory response and production of reactive oxygen species (ROS), which affects the organs remote to the sites of I/R. The aim was to assess the hepatic changes after renal I/R injury. MATERIALS AND METHODS: Twenty mice were subjected to either sham operation or varying degrees of renal I/R injury. Hepatic TNF-alpha levels, myeloperoxidase (MPO), superoxide dismutase (SOD), and catalase (CAT) activities and reduced glutathione (GSH) levels, thiobarbituric acid-reactive substances (TBARS), and protein carbonyl levels were evaluated to show hepatic response to renal I/R injury. RESULTS: Hepatic tumor necrosis factor-alpha levels were found to be increased significantly after 30 min ischemia-1 h reperfusion and remained elevated through 60 min ischemia-1 h reperfusion. Supporting the neutrophil recruitment, about 10-fold increase in MPO activity was detected after 30 min ischemia-1 h reperfusion. Antioxidant enzymes were detected to be decreased after 30 min ischemia-1 h reperfusion and reached to the minimum levels after 60 min ischemia-1 h reperfusion. Decreased levels of GSH and increased levels of TBARS and protein carbonyls after 60 min ischemia-1 h reperfusion supported the ROS-mediated biomolecular alterations. CONCLUSIONS: A minumum of 30 min ischemia-1 h reperfusion is enough to elicit remote effects of renal I/R injury. Care should be taken to protect other organs remote from I/R sites especially during renal surgery.

Animals↗

Lipid peroxidation in rat brain during focal cerebral ischemia: prevention of malondialdehyde and lipid conjugated diene production by a novel antiepileptic, lamotrigine.

The effects of Lamotrigine (LTG) which blocks ischemia induced glutamate (Glu) release, on lipid peroxidation have been evaluated in cortical and cerebellar tissues of rat brain during focal cerebral ischemia. A total of 45 rats were randomly assigned into one of four groups; sham operated animals as controls, animals subjected to middle cerebral artery occlusion (MCAO) and treatment groups with LTG (20 mg/kg i.p.) either 30 min before or just after MCAO. Changes in lipid peroxides were expressed as nanomoles of malondialdehyde (MDA) and conjugated diene (CD) per milligram of protein. MDA values following 60 min of ischemia relative to contralateral cortex and CD levels in 0, 10 and 60 min of ischemia were found to be higher in the ipsilateral cortex than those in the contralateral cortex. On the other hand, contralateral cerebellar MDA levels after 0 and 60 min of ischemia and CD levels after 0, 10 and 60 min of ischemia were higher than those in the ipsilateral cerebellum. Pharmacological inhibition of Glu release significantly decreased the MDA and CD production in both cortex and cerebellum. Pre- or post-ischemic administration of LTG did not significantly change CD levels, but MDA levels in contralateral cortex were found to be significantly decreased than those in ischemic cortex in both pre- and post-treated group.

Animals↗

The effects of NMDA receptor antagonist MK-801 on lipid peroxidation during focal cerebral ischemia in rats.

The effect of MK-801 on ischemic neuronal damage was studied in a rat model of permanent focal cerebral ischemia in terms of ipsilateral and contralateral cortical and cerebellar tissue lipid peroxides. Forty-five male Swiss Albino rats were assigned into one of four groups: sham operated as controls, subjected to right middle cerebral artery occlusion (MCAO) or injection of MK-801 (0.5 mg/kg i.p.) either 30 min before or just after right MCAO. Changes in lipid peroxides were expressed as nmol malondialdehyde (MDA) and conjugated diene (CD)/mg protein. MDA values after 60 min of ischemia relative to contralateral cortex and CD levels in 0, 10 and 60 min after ischemia were found to be higher in ipsilateral cortex than those in contralateral cortex. On the other hand, contralateral cerebellar MDA levels in 0 and 60 min of ischemia and CD levels in 0, 10 and 60 min after ischemia were found to be higher than those in ipsilateral cerebellum. Pharmacological inhibition of glutamate receptor by MK-801 before or just after permanent MCAO decreased significantly the MDA and CD levels in both cortex and cerebellum. Although no significant differences found in MDA values between rats pre- and posttreated with MK-801, CD levels in posttreated group seemed significantly lower than those in pretreated group. On the whole, these results suggest that MDA and CD represent early biochemical marker of lipid peroxidation in ischemic tissues, reflecting the radical-mediated tissue damage.

Alkenes↗

Determination of cut-off values for leucocytes and bacteria for urine flow cytometer (UF-100) in urinary tract infections.

Leucocytes and bacteria in urine are the important indices for diagnosing urinary tract infections. Urine specimens from 260 patients were examined for leucocytes and bacteria with the UF-100 flow cytometer (Sysmex Corporation, Japan). The results obtained with the UF-100 were compared with those obtained by bacteriologic cultures of the same urine samples. Bacteriologic samples were found to be positive in 48 urine samples. The best detected cut-off value for bacteria is 3800/microL (senstivity = 73%, specificity = 78%) and 25/microL for leucocytes (sensitivity = 73%, specificity = 92%). In addition, comparison of leucocyte count by manually and with UF-100 shows good correlation (r = 0.91). A flow cytometric urinalysis analyzer operates in a time saving manner, increases throughput and decrease microscopy review rates. It also provides a reliable information to clinicians prior to bacteriologic culture results, in terms of leucocyte and bacteria count.

Bacteriuria↗

Oxidative stress markers in hepatitis C infected hemodialysis patients.

BACKGROUND: Oxidative stress in hemodialysis (HD) patients or hepatitis C virus (HCV) infections may be related to increased production of free radicals. We assessed the effect of HCV infection on the oxidative stress markers, malondialdehyde (as TBARS), protein carbonyl content and protein sulfhydryl groups, in chronic HD patients. METHODS: Twenty HCV infected patients (9 men and 11 women, age 44.8 +/- 14.3 years) and 10 non-HCV infected patients (6 men and 4 women, age 55.6 +/- 14.3 years) receiving regular HD were recruited. The average hemodialysis duration was 30 +/- 8 months for HCV (+) patients and 14 +/- 8 months for HCV (-) patients. Controls consisted of healthy subjects. RESULTS: Serum TBARS and carbonyl content were significantly elevated in HCV(-) patients (p<0.001, p<0.05) and in HCV(+) patients (p<0.001, p<0.001) vs. Controls. There was also a significant difference in serum TBARS and carbonyl content between HCV(-) patients and HCV(+) patients (p<0.001, p<0.05). Serum protein sulfhydryl groups in HCV(-) and HCV(+) patients were the same, but significantly lower than in Controls (p<0.001, p<0.001). When HCV(+) patients were divided into two sub-groups, one with shorter (13.4 +/- 8 months; n=7) and the other with longer (40.3 +/- 8 months; n=13) duration of HD treatment, no differences were found between subgroups. CONCLUSION: HCV infection may aggravate oxidative stress in HD patients.

Adult↗

Protective effect of quercetin on renal ischemia/reperfusion injury in rats.

BACKGROUND: There is increasing evidence to suggest that toxic oxygen radicals play a role in the pathogenesis of ischemia/reperfusion (I/R) injury in the kidney. The aim of this study was to evaluate whether quercetin, an oxygen free radical scavenger, protects kidney tissue. METHODS: A renal I/R injury was induced by a left renal pedicle occlusion by ischemia for 45 min, followed by 60 mins of reperfusion with contralateral nephrectomy in rats. The rats were pretreated intraperitoneally with a quercetin suspension (50 mg/kg) 60 min before the ischemia induction. Thiobarbituric acid reactive substances (TBARS), protein carbonyl content, tumor necrosis factor alpha (TNF-alpha), reduced glutathione (GSH) levels, myeloperoxidase (MPO) catalase (CAT) and superoxide dismutase (SOD) activities were determined in renal tissue. RESULTS: There were 3 groups of rats, the control group, the I/R group and the I/R+Q group. Our results indicate that TBARS, TNF-alpha levels, MPO activity and protein carbonyl content were significantly higher in the I/R group than those in the control group (p<0.05, p<0.01, p<0.01 and p<0.01, respectively). Quercetin administration significantly decreased these parameters (p<0.05, p<0.01, p<0.05 and p<0.01, respectively). GSH levels, SOD, and CAT activities significantly decreased after I/R injury when compared to the control group (p<0.01, p<0.05 and p<0.01, respectively). Quercetin treatment significantly increased GSH levels and activities of these enzymes when compared to the I/R group (p<0.05, p<0.01, p<0.05, respectively). CONCLUSIONS: These results suggest that quercetin reduces renal oxidative injury and facilitates repair. Quercetin can have a role in a renoprotective therapeutic regimen.

Animals↗

Expression and distribution of aquaporin-1 in nasal polyps: does it have any significance in edema formation?

BACKGROUND: The aim of this study was to investigate the expression of Aquaporin 1 (AQP1) and AQP4 in polyp tissue. METHODS: Nasal polyps were obtained from 34 patients with nasal polyposis during endoscopic sinus surgery. Bullous middle turbinates with normal-appearing mucosa of 10 patients were used as controls. Expression of AQP1 and AQP4 water channels were determined by immunohistochemical methods. RESULTS: AQP1 has been found to be expressed in fibroblasts located in polyp tissue, especially in the subepithelial area, periphery of seromucous glands, and endothelial cells of venules. CONCLUSION: We have established a high expression of AQP1 water channels in nasal polyp tissue and have suggested two mechanisms to explain this finding. Increased AQP1 expression may be a cause or a consequence of edema formation. Thus, additional studies are needed to elucidate the true mechanism underlying this relationship.

Aquaporin 1↗