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Biomedical subjects

K Kilinç

Publications and source records attributed to K Kilinç.

50 records · Page 3Linked to original sources

The effect of allopurinol pretreatment before detorting testicular torsion.

The resumption of blood flow to organs following ischemia may cause a further increase in tissue damage through an increase in peroxidation of lipids in cell membranes. An experimental study was conducted to investigate the prevention of reperfusion injury after testicular torsion through changes in the lipid peroxide content of the testis. Adult male albino rats were divided into 11 groups, each containing 10 rats. One group served to determine base values of the lipid peroxide content of the testis and kidney; 3 groups were subjected to unilateral testicular torsion lasting 1, 3 and 5 hours; 3 groups were subjected to detorsion following torsion lasting 1, 3 and 5 hours; 3 groups were treated with allopurinol before detorsion following torsion lasting 1, 3 and 5 hours; and 1 group underwent sham operation as a control. Thiobarbituric acid reactive products of lipid peroxidation (TBAR) were assessed in testicular and renal tissues. Testicular torsion caused a significant increase in TBAR in the testis (p < 0.01), but not in the kidneys. Detorsion caused a further significant increase in testicular TBAR (p < 0.01). Pretreatment with allopurinol prevented this further increase (p < 0.01). It is concluded that, biochemically, reperfusion injury occurs in the testis following detorsion after testicular torsion of 720 degrees lasting as long as 5 hours. Pretreatment with allopurinol before detorsion prevents such reperfusion injury.

Allopurinol↗

Ipsilateral and contralateral testicular biochemical acute changes after unilateral testicular torsion and detorsion.

OBJECTIVES: An experimental study has been conducted to investigate testicular blood flow alterations through acute biochemical changes during unilateral testicular torsion and detorsion. METHODS: One hundred twenty male albino rats were divided into 12 groups, each containing 10 rats. One group served to determine basal values of biochemical parameters, 4 groups were subjected to varying periods of unilateral testicular torsion (3, 6, 12, and 24 hours, respectively), 3 groups were subjected to detorsion following varying periods of torsion (6, 12, and 24 hours, respectively), and 4 groups underwent sham operations as controls. Levels of lactic acid, hypoxanthine, and lipid peroxidation products were determined in testicular tissues. RESULTS: Values of these 3 parameters obtained from sham operation control groups did not differ significantly from basal values (p > 0.05). All 3 parameters were increased significantly in both ipsilateral torted and contralateral nontorted testes after unilateral testicular torsion when compared with basal values (p < 0.05). Detorsion did not cause significant changes in levels of lipid peroxidation products in both ipsilateral torted and contralateral nontorted testes when compared with values obtained after torsion (p > 0.05). CONCLUSIONS: Ipsilateral testicular torsion causes a decrease not only in the ipsilateral torted but also in the contralateral nontorted testicular perfusion. The clues of reperfusion injury do not become evident following detorsion of testicular torsion lasting more than 6 hours.

Animals↗

The preventive role of chemical sympathectomy on contralateral testicular hypoxic parameters encountered during unilateral testicular torsion.

OBJECTIVE: To evaluate the effect of chemical sympathectomy on lactic acid and hypoxanthine concentrations in both testes during unilateral testicular torsion in a rat experimental model. MATERIALS AND METHODS: Four groups, comprising 10 rats each, were studied. Group I was the control group, Group II rats received a placebo and underwent unilateral testicular torsion, Groups III and IV received guanethidine monosulphate and 6-OH-dopamine hydrobromide respectively, and underwent unilateral testicular torsion. The levels of lactic acid and hypoxanthine in both testes were measured. RESULTS: In rats in Group II the levels of lactic acid and hypoxanthine in both testes were significantly elevated when compared to the control group. In the groups of rats that had undergone chemical sympathectomy, the levels of lactic acid and hypoxanthine were significantly decreased in the contralateral testes compared to rats in Groups I and II. CONCLUSION: Chemical sympathectomy prevents the elevation of lactic acid and hypoxanthine levels in the contralateral testis of rats with unilateral testicular torsion. Therefore, we conclude that contralateral testicular damage during unilateral testicular torsion may result through a reflex activating sympathetic system.

Animals↗

Reperfusion injury after detorsion of unilateral testicular torsion.

Reperfusion injury has been well documented in organs other than testis. An experimental study was conducted to investigate reperfusion injury in testes via the biochemical changes after unilateral testicular torsion and detorsion. As unilateral testicular torsion and varicocele have been shown to affect contralateral testicular blood flow, reperfusion injury was studied in both testes. Given that testicular blood flow does not return after 720 degrees testicular torsion lasting more than 3 h, the present study was conducted after 1 and 2 h of 720 degrees torsion. Adult male albino rats were divided into seven groups each containing ten rats. One group served to determine the basal values of biochemical parameters, two groups were subjected to 1 and 2 h of unilateral testicular torsion respectively, two groups were subjected to detorsion following 1 and 2 h of torsion respectively, and two groups underwent sham operations as a control. Levels of lactic acid, hypoxanthine and lipid peroxidation products were determined in testicular tissues. Values of these three parameters obtained from the sham operation control groups did not differ significantly from basal values (P > 0.05). All three parameters were increased significantly in both ipsilateral and contralateral testes after unilateral testicular torsion when compared with basal values (P < 0.01 and P < 0.05, respectively). Detorsion caused significant changes in lipid peroxidation products levels in ipsilateral but not in contralateral testes when compared with values obtained after torsion (P < 0.01 and P > 0.05, respectively). It is concluded that ipsilateral testicular torsion causes a decrease in perfusion not only in the ipsilateral but also in the contralateral testis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Lipid peroxide level increase in experimental hydrocephalus.

The aetiology of incomplete adrenergic denervation and reduction in the number and caliber of the cerebral vessels in hydrocephalus is still obscure. Stretching of the blood vessels alone is far from explaining these major vascular changes. Previous studies have shown that increased lipid peroxidation produces toxic effects on vessels. This experimental study was designed to investigate the possible aetiology of vascular changes in hydrocephalic rats with special reference to lipid peroxidation. Hydrocephalus was induced by injecting 50 mg/Kg sterilized kaolin suspension into the cisterna magna in 10 rats (Group A). A sham operation was performed for Group B. After three weeks the rats were anaesthetized and perfused transcardially. The brains were dissected, and cut to visualize the degree of hydrocephalus. The arteries of the circle of Willis were removed for light microscopic examination and the brains were kept for the measurement of lipid peroxidation levels. Light microscopic studies of cerebral arteries in hydrocephalic rats revealed spastic vessels with folding and corrugation of the lamina elastica. The level of lipid peroxidation in group A (260 +/- 9.129 nmol TBAR/gr wet tissue) was significantly higher than that of group B (106 +/- 3.59 nmol TBAR/gr wet tissue). It is suggested that vascular changes observed in hydrocephalic rats may be due to the high level of lipid peroxidation, which in turn may be the consequence of ischaemia caused by the hydrocephalus related stretching of cerebral vessels.

Animals↗

Cobaltous ion inhibition of lipid peroxidation in biological membranes.

The effect of cobalt on lipid peroxidation in biological membranes, phospholipid liposomes and fatty acid micelles was investigated. Cobaltous ion, at micromolar concentrations, inhibited iron-ascorbate induced lipid peroxidation in erythrocyte ghosts, microsomes and phosphatidylserine liposomes at pH 7.4. The pH seemed to be important for the anti-peroxidative effect of cobalt, because under slightly acidic conditions cobalt did not inhibit peroxidation. Cobalt was less effective in inhibiting peroxidation stimulated by organic hydroperoxides. Iron-ascorbate induced lipid peroxidation was also inhibited by EDTA. However, certain ratios of EDTA: cobalt in the reaction mixture stimulated peroxidation. Cobalt did not inhibit lipid peroxidation in linoleic acid micelles and phosphatidylethanolamine liposomes. The presence of phosphatidylserine, however, rendered these micelles and liposomes to cobalt inhibition. We conclude that the cobaltous ion is a potent inhibitor of lipid peroxidation in biological membranes and that the binding of cobalt to phosphatidylserine is necessary for the inhibitory effect of this metal ion.

Animals↗

The role of lipid peroxidation in the genesis of vasospasm secondary to subarachnoid hemorrhage.

The aim of this study is to find out the possible trigger role of lipid peroxidation in vasospasm. Haemoglobin-free washed erythrocyte membranes (erythrocyte ghost) corresponding to 2.5 mg membrane protein was mixed with 0.5 umol NADPH 3 umol ADP, 4 umol ferrous sulphate and injected into the cisterna magna of cats to stimulate lipid peroxidation in vivo (Group 1). The second group was injected lml/kg whole blood and the control group 1 ml/kg saline. Angiographic studies revealed significant vasospasm in five cats in group 1. Severe vasospasm was seen in six cats in group 2. A significant increase in lipid peroxidation was observed in groups 1 and 2, compared to the control group. These results may suggest that free radical products may play an important role in the complex genesis of vasospasm in subarachnoid haemorrhage.

Angiography↗

Irreversible inactivation of human erythrocyte pyruvate kinase by 2,3-butanedione.

Human erythrocyte pyruvate kinase was found to be irreversibly inactivated by butanedione in the dark. The second-order rate constants for inactivation at pH 8.0 and 25 degrees C were 2.14 and 2.74 M-1 min-1 in the absence and presence of 50 mM borate, respectively. The pH profile of the inactivation indicated the involvement of a residue with an apparent pK alpha of 8.1-8.3. ADP and phosphoenolpyruvate acted as partial inhibitors of the inactivation process. Certain details of the inactivation, spectral studies, and fluorometric determinations gave evidence for arginine as the only target residue. A total of 23 +/- 3 residues per subunit were modified within the period required for inactivation. In the same period the presence of 4 mM ADP reduced the extent of inactivation by 70% and the number of modified residues to 18 +/- 4. The number of the arginine residues protected by ADP from butanedione modification was 5.0 +/- 1.3 per subunit.

Adenosine Diphosphate↗

A rapid purification method for human erythrocyte pyruvate kinase.

Human erythrocyte pyruvate kinase (ATP: pyruvate phosphotransferase, E.C.2.7.1.40) is purified 30,000-fold, using a method which includes ammonium sulfate precipitation, Sephadex G-75 filtration, and Blue Dextran-Sepharose 4B chromatography. The enzyme is resolved into two peaks on Blue Dextran-Sepharose 4B. The first peak with sp act of 300 corresponds to the mature form (R4) whereas the second peak with sp act of 180 corresponds to R2R'2. Peaks I and II give one band on 10% polyacrylamide gel without SDS. Peak II gives two bands on 10% SDS gel with molecular weights 60,000 (R') and 57,500 (R). On the other hand, peak I gives only one band on 10% SDS gel having a molecular weight of 57,500. Both the R4 and R2R'2 forms of the enzyme have the same pH optimum of 7.2.

Chemical Phenomena↗

Effects of intra-articular vitamin E and corticosteroid injection in experimental hemarthrosis in rabbits.

The effects of intra-articular injections of vitamin E and corticosteroid were investigated in skeletally mature New Zealand white rabbits in which experimental hemarthrosis was induced for 14 days. The rabbits were divided into three groups composed of eight rabbits each: the first group comprised of animals with hemarthrosis, the second group animals with hemarthrosis and intra-articular injections of 20 mg vitamin E, and the third group animals with hemarthrosis and intra-articular injections of 10 mg of triamcinolone acetonide (TCA). Proteoglycan levels in the joint cartilage of the hemarthrosis group were found to be increased significantly compared with the controls (P < .01), whereas in the vitamin E-injected group they were significantly decreased (P < .05). In the TCA-injected group, proteoglycan levels were not found to be significantly different from those in the hemarthrosis group (P > .05). Histopathological evaluation showed that the cartilage structure in the joint of the control limbs was identical to that in the vitamin E- and TCA-injected limbs. In the hemarthrosis group, in comparison with the controls, the joint surface was roughened and fibrillated. In the superficial areas of the cartilage tissue, chondrocytes were decreased in number. These findings suggest that in this model, vitamin E and TCA may be helpful in preventing the joint cartilage changes seen in hemarthrosis.

Animals↗

Serum levels of eosinophilic cationic protein (ECP), myeloperoxidase (MPO), lipid peroxidation products, interleukin (IL)-5 and interferon (IFN)-gamma in children with bronchial asthma at acute asthma attack and remission.

We determined serum levels of myeloperoxidase (MPO), eosinophilic cationic protein (ECP), reactive oxygen species measured as thiobarbituric acid reactive substances (TBARS), interleukin (IL)-5, and interferon (IFN)-gamma in 14 asthmatic children during an asthma attack and remission. Twelve healthy children served as controls. In atopic asthmatics, asthma attack resulted insignificant elevations of ECP, MPO, and TBARS compared to remission. TBARS levels were also higher at remission compared to controls. However, there was a great deal of overlap in the values of asthmatics and controls. IL-5 and IFN-gamma were detectable at low levels and only in a few patients. These results provide further evidence for participation of eosinophils, neutrophils and reactive oxygen species in the pathogenesis of acute asthma, and suggest that their products may be used in monitoring asthma attack. Serum IL-5 and IFN-gamma levels are not appropriate for use in the follow-up of asthmatic children.

Acute Disease↗

Serum levels of antioxidant vitamins (alpha tocopherol, beta carotene, and ascorbic acid) in children with bronchial asthma.

We determined serum levels of alpha tocopherol, beta carotene, and ascorbic acid and lipid peroxidation products (thiobarbituric acid reactive substances--TBARS) in 14 children during an asthma attack and remission. Twelve healthy children served as controls. All antioxidant vitamins were significantly lower in asthmatics at remission compared to controls. Comparison of attack and remission periods in asthmatic patients failed to reveal any difference except in beta carotene (p = 0.03). The levels of all three vitamins correlated very significantly with each other (r = 0.89-0.95). TBARS levels were significantly higher at asthma attack compared to remission (p = 0.001). No correlation was observed between the antioxidant vitamins and lipid peroxidation products. This study shows that antioxidant vitamins are decreased in sera of asthmatic patients even during the asymptomatic periods of the disease, and that this decrease is not totally dependent on the increased oxidative stress as reflected by lipid peroxidation products. The role of antioxidant vitamins in prevention and/or treatment of asthma remains to be determined.

Adolescent↗

Serum lipid peroxidation levels in small-for-gestational-age babies.

The levels of lipid peroxidation in sera of asymmetric small-for-gestational-age (SGA) babies at the second hour of life were investigated. Lipid peroxidation levels, measured as malondialdehyde (MDA), were 3.3 +/- 1.1 and 3.9 +/- 1.2 mmol/L in SGA and appropriate-for-gestational age (AGA) groups, respectively. The difference was not significant (p>0.05). This result may indicate that free radical scavengers are sufficient in SGA babies.

Biomarkers↗

Serum malondialdehyde concentration as a measure of oxygen free radical damage in preterm infants.

Lipid peroxidation was measured in 35 preterm infants by determining serum malondialdehyde (MDA) levels during the fist week of life. Serum concentrations of MDA were measured at one hour, 24 hours, 48 hours and one week of age. There were no correlations between gestational age, birth weight, and serum malondialdehyde levels at one, 24, or 48 hours, or on day seven. Serum MDA levels were higher in infants requiring mechanical ventilation compared to those breathing spontaneously, but the difference was not statistically significant. There were no correlations between MDA levels and corresponding fraction of inspired oxygen (FiO2) levels and arterial oxygen tension. No significant difference in serum MDA concentration was seen in relation to intravenous feeding with lipid emulsions. Serum MDA concentrations of infants with sepsis were not different at hours one, 24 and 48, but were significantly higher on day seven, when compared with infants without sepsis. MDA levels in the first and second serum samples were significantly higher in infants who were born after spontaneous vaginal delivery, compared to those born by cesarean section.

Age Factors↗