Biomedical subjects

U K Sentürk

Publications and source records attributed to U K Sentürk.

18 recordsLinked to original sources

PubMed2006

Plasma levels of nitrites, PGF1alpha, and nitrotyrosine in LPS-treated rats: functional and histochemical implications in aorta.

We investigated the effects of lipopolysaccharide (LPS) administration on plasma nitrite, nitrotyrosine and 6-keto prostaglandin F1alpha, (PGF1alpha) levels and the related resultant changes in function and histochemistry of aorta in rats. Plasma nitrite and PGF1alpha nitrotyrosine levels were analysed after 5 mg/kg intravenous LPS was administered to rats compared with those in non-treated rats. The distribution of nitrotyrosine in the aorta was studied immunohistochemically. The contractile responses of aortic rings to phenylephrine (PE) from both the LPS-treated and control rats were studied in the organ baths. There were increases in plasma nitrite, PGF1alpha, and nitrotyrosine concentrations of LPS-treated rats compared to non-treated rats. Immunoreactivity of nitrotyrosine residues were detected in the endothelial and smooth muscle cells in LPS-treated but not in control rat aorta. The contractile responses to PE of the LPS-treated rat aortic rings were significantly reduced as compared with those of control rat's. Incubation of the aortic rings from LPS-treated rats with cyclooxygenase inhibitor indomethacine or with a combination of indomethacine and nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) increased the contractile responses to the levels observed in control rats suggesting that both prostanoids and particularly nitric oxide (NO) are involved in the reduced contractile responses in LPS-treated rats. These results supported the view that LPS might cause an increment in both NO and PGI2 levels. This increase in the NO and PGI2 levels may be responsible from the reduction in responses of aorta to contractile agents in LPS-treated rats. Increased peroxynitrite formation in LPS-treated rats may lead to nitration of the tyrosil residues of the proteins in the aorta.

Animals↗

PubMed2005

Angiotensin II inhibition attenuates postexercise proteinuria in rats.

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.

Angiotensin II↗

PubMed2004

The effect of one year's swimming exercise on oxidant stress and antioxidant capacity in aged rats.

The effect of exercise on oxidant stress and on alterations in antioxidant defense in elderly has been investigated extensively. However, the impact of regularly performed long-term physical activity starting from adulthood and prolonged up to the old age is not yet clear. We have investigated the changes in the activities of antioxidant enzymes - superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) - and lipid peroxidation in various tissues of rats which had performed (old-trained) or had not performed (old-control) regular swimming exercise for one year. These animals were compared with young-sedentary rats. Increased lipid peroxidation was observed with ageing in all tissues (heart, liver, kidney, striated muscle) and swimming had no additional effect on this elevation of lipid peroxidation. Heart and striated muscle SOD activites, and striated muscle CAT activity increased as a consequence of ageing, whereas kidney and liver CAT activities, as well as GPx activities in kidney, liver, lung and heart were significantly decreased compared to young controls. Lung and heart SOD, liver CAT activities as well as GPx activities in liver, lung and heart were increased significantly in rats which performed exercise during ageing, compared to the old-control group. These findings suggest that lifelong exercise can improve the antioxidant defense in many tissues without constituting any additional oxidant stress.

Aging↗

PubMed2001

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats.

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.

Animals↗

PubMed2000

Effect of long-term swimming exercise on somatosensory evoked potentials in rats.

The study investigated whether long-term swimming exercise prevents age-related changes in rat somatosensory evoked potentials (SEPs) and somatosensory cortex (SC) morphology. A total of 25 9-month-old rats were assigned to an exercise or control group. The exercise group swam 1 h/day five times weekly for 1 year. The results showed that long-term exercise prevented age-related changes in SEPs and SC morphology.

Animals↗

PubMed2000

Tissue and blood levels of zinc, copper, and magnesium in nitric oxide synthase blockade-induced hypertension.

The aim of this study was to determine the levels of tissue and blood zinc (Zn), copper (Cu), magnesium (Mg) in nitric oxide (NO) synthase blockade-induced hypertension. A group of albino rats received a NO synthase inhibitor, N(G)-nitro-L-arginine-methyl ester (L-NAME, 60 mg/kg/d) in their drinking water for 21 d. L-NAME intake caused a progressive rise in this group's resting mean arterial blood pressure compared to a control group (p < 0.01). There were no differences between the groups with regard to tissue and blood levels of Zn or Cu; however, Mg concentrations were significantly lower in the hypertensive rats' erythrocytes (20.2% reduction from control levels), cerebral cortex (17.0%), heart (9.1%), renal cortex (12%), renal medulla (16.7%), and in the tissues of the caval vein (23.7%), mesenteric artery (29.8%), renal artery (18.4%), and renal vein (22.1%). There were no significant Mg concentration changes in the hypertensive group's plasma, cerebellum, liver, duodenum, or aortal tissue. These findings suggest that Mg depletion may play a role in the blood pressure rise that occurs in the model of chronic NO synthase inhibition-induced hypertension.

Animals↗

PubMed2000

The effect of pre and postnatal cadmium exposure on somatosensory evoked potentials: relation to lipid peroxidation.

Pregnant swiss albino rats were divided into three groups: control (C), gestational exposure of cadmium (G-Cd) and gestational/postnatal exposure of cadmium (GP-Cd) groups. Control animals received tap water and the rats of GP-Cd group received Cd as CdCl2 in their drinking water during the experimental period. G-Cd group was given Cd during pregnancy, but given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be treated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an additional 38 days. On postnatal day (PND) 60, somatosensory evoked potentials (SEPS) of three groups were recorded following left posterior tibial nerve (PTN) stimulation. The mean latencies of N1, P1, and N2, components were significantly prolonged in both Cd groups compared with control group. The mean latency of N1 in the GP-Cd group was longer than control and the G-Cd groups. There was no significant amplitude differences among groups. On the other hand, thiobarbituric acid reactive substances (TBARS), an indicator of lipid peroxidation, were increased in the sciatic nerves of both groups compared with control group. A significant increase in the TBARS level of the brain was found only in GP-Cd group due to significant accumulation of Cd.

Age Factors↗

PubMed1999

Effect of cadmium-induced lipid peroxidation on EEG spectral components.

Pregnant Swiss albino rats were divided into control (C) and cadmium (Cd) groups. Control animals received tap water while the Cd group received Cd as CdCl2 in their drinking water. The rat pups were separated from their mothers 22 days after birth. 78 young rats were divided into two main groups: controls (C1, C2, C4) and cadmium groups (Cd1, Cd2, Cd4). Each sub-group included 13 rats. On postnatal days 30, 60, and 120, spectral analysis of EEGs recorded from the parietal lobes of all groups of rats was computed by fast Fourier transform (FFT) algorithm. The amplitude maxima were found to occupy the frequency bands of 1-2, 2-4, 4-6, 6-8, 8-16, and 16-30 Hz. The decibel (dB) values of the maxima were significantly decreased in Cd1 and Cd2 groups compared with the corresponding control groups in all the frequency bands except 16-30 Hz. A significant amplitude (dB) decrease was observed in all the frequency bands of the Cd4 group compared with the C4 group.

Animals↗

PubMed1996

The effect of manganese-induced hypercholesterolemia on learning in rats.

Since the exact mechanism of manganese (Mn)-induced learning disability is not known, we investigated the role of elevated cholesterol in rats exposed daily to 357 and 714 micrograms Mn/kg for 39 d. Significant Mn accumulation was accompanied by increased cholesterol content in the hippocampal region of Mn-treated rats. The learning, which is based on the time needed to reach food placed at the exit of a T-maze after a 1-d training period, was significantly slower in exposed rats than in unexposed rats. The rats receiving 357 and 714 micrograms Mn/kg reached the food in 104.5 +/- 13.8 and 113.3 +/- 25.7 s, respectively, on d 30, whereas their untreated counterparts reached the food in 28.7 +/- 11.4 s. This delay was completely corrected to 29.3 +/- 7.8 and 30.7 +/- 6.0 s in rats with coadministration of an inhibitor of cholesterol biosynthesis with 357 and 714 micrograms/kg of Mn. The correction of impaired learning was associated with the normalization of hippocampal cholesterol, but the Mn level in this region of the brain was not influenced in rats treated with a drug that inhibits cholesterol biosynthesis. These results suggested that Mn-induced hypercholesterolemia is involved in Mn-dependent learning disability.

Administration, Oral↗

PubMed1996

Comparison of Tc-99m HIG and Ga-67 citrate in the evaluation of bacterial abscess in a rat model.

Tc-99m labeled polyclonal human immunoglobulin (HIG) has been shown to be able to localize an inflammatory site. There are several possible explanations for HIG accumulation at focal infection sites such as increased vascular permeability, binding of the Fc part of Ig to Fc receptors of leucocytes and binding directly to bacteria. In this study, we compared Tc-99m HIG and Ga-67 citrate scintigraphy in localizing acute bacterial abscesses induced by E. coli and S. aureus. Serial scintigrams were performed at 1, 4, 24 hr after injection. Tc-99m HIG showed greater accumulation at all times with both infections agents than Ga-67 citrate (p < 0.05). While Tc-99m HIG showed greater accumulation in S. aureus than E. coli (p < 0.05), there was no statistically significant difference between E. coli and S. aureus (p > 0.05) by Ga-67 citrate. Our study suggests that Tc-99m HIG is a superior agent to Ga-67 and bacterial affinity can be a factor responsible for HIG accumulation at focal sites of inflammation.

Abscess↗

PubMed1996

Role of cadmium-induced lipid peroxidation in the kidney response to atrial natriuretic hormone.

In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 micrograms/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 +/- 7.0 and 81.2 +/- 3.8 mm Hg to 128.1 +/- 4.6 and 107.9 +/- 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creatinine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 +/- 64.1 to 303.3 +/- 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 micrograms/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.

Animals↗

PubMed1995

The role of cadmium in the peroxidative response of kidney to stress.

Since the kidney is a main target for cadmium, its accumulation in the kidney tissue by increasing peroxidative damage make the kidney functions vulnerable to stress. For this reason, the effect of cadmium-induced peroxidative damage to kidney responses to stress was investigated in this study. Two-month-old albino rats receiving 15 micrograms/mL containing Cd drinking water for 30 d were exposed to restraint and cold stress for 6 h, and their responses were compared with those of unstressed counterparts. Lipid peroxidation was found to be significantly higher in the cortical portion of kidney in cadmium-exposed rats than that of unexposed animals. The mean thiobarbutyric acid reactive substance (TBARS) level rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p < 0.01). Six hours of cold and restraint stress caused an elevation in the cortical TBARS level in control animals without affecting its level in cadmium-exposed rats. Despite unaltered cortical TBARS, its medullar levels increased significantly in cadmium-exposed rats because of stress. These results suggested that cadmium accumulation in the kidney increases the susceptibility of medulla against peroxidative damage. However, further functional studies are necessary to explain the role of cadmium in the stress-induced deterioration of medullar functions.

Animals↗

PubMed1995

Reversibility of manganese-induced learning defect in rats.

In this study the mechanism by which manganese (Mn) induces learning defect and its reversibility has been investigated in rats. Female albino rats were dosed orally with 357 micrograms Mn/kg body weight for 15 or 30 days. Attempts were made to correct the Mn-induced learning defect by (1) co-administration of mevinolin and Mn for 30 days; (2) administration of mevinolin for 15 days after 15 days of dosing with Mn, and (3) by withdrawal of Mn treatment (15 days dosing with Mn followed by 15 days without Mn). Mevinolin was given orally at 235.7 micrograms/kg body weight. Significant increases in the Mn and cholesterol levels in the hippocampus were accompanied by an obvious slowness in learning of rats exposed to Mn. After one training period (day 29) the time required to reach the exit of a T-maze was 104.5 +/- 13.8 sec for rats dosed with Mn for 30 days, whereas that of the controls was 28.7 +/- 11.4 sec on day 30. This delay was completely corrected (to 30.7 +/- 6.0 sec) in rats co-administered mevinolin (an inhibitor of cholesterol biosynthesis) with Mn. Withdrawal of Mn, with or without inhibiting the cholesterol biosynthesis, also corrected the Mn-induced learning defect. These results suggest that Mn toxicity produces learning disability by increasing cholesterol biosynthesis and this reversible disability in learning can be corrected by withdrawal of Mn exposure.

Administration, Oral↗

PubMed1995

Cyclosporin A affects red blood cell deformability in vivo but not in vitro in guinea pig.

A hemorheological mechanism has been proposed for the hemodynamic effects of cyclosporin A (CsA). In vivo and in vitro effects of CsA on red blood cell (RBC) deformability were investigated in guinea pigs. RBC transit time, measured by a cell transit analyzer, was found to be prolonged, implying impaired deformability in guinea pigs treated with CsA (10 mg/kg/day) for 7 days. Blood CsA concentration was approximately 900 ng/ml. RBC cytosolic calcium concentration was higher in the CsA-treated groups than in the control group. RBC lipid peroxidation was not affected. Combining pentoxifylline injections (100 mg/kg/day) with CsA therapy did not prevent the effect on RBC deformability and cytosolic calcium concentration. CsA did not affect RBC transit time and cytosolic calcium concentration in vitro. Thus, the influence of CsA on RBC deformability appears to be an indirect effect that is mediated by the alterations in RBC calcium homeostasis.

Animals↗

PubMed1994

Role of lipid peroxidation in cadmium-induced impairment of the gastric mucosal barrier.

Peroxidative tissue damage has been reported to contribute to several pathological disorders. Despite high exposure to both exogenous and endogenous oxidant stress, the strong cell defence mechanism of the gastric mucosa protects mucosal epithelial cells against these noxious stimuli. However, some environmental factors involved in lipid peroxidation (such as cadmium), which disrupt gastric mucosal protection, may impair the mucosal barrier and facilitate the occurrence of gastric ulcers. In an experimental study to investigate this hypothesis, the level of cadmium-induced lipid peroxidation products (TBARS) and an antioxidant enzyme (SOD) were investigated. The mucin content (P < 0.01) and prostaglandin levels (P < 0.05) of mucosa as components of the gastric mucosal barrier were found to be significantly reduced in rats exposed to 15 ppm of cadmium in water for 30 days when compared with those of unexposed controls. TBARS levels in blood (P < 0.05) and mucosa (P < 0.001) increased markedly in cadmium-exposed animals whereas blood SOD levels remained unchanged. The significant correlation between TBARS and mucosal cadmium (r = 0.664, P < 0.01), as well as between cadmium and PGE2 (r = -0.719, P < 0.01), led to the conclusion that cadmium-induced lipid peroxidation is involved in the increased vulnerability of gastric mucosa to injurious stimuli in rats. This susceptibility may be responsible for the high incidence of stress-induced gastric ulcer in the population.

Animals↗

PubMedDate not supplied

The susceptibility to stress-induced gastric injury of rats exposed to cadmium.

In this experimental study, the effect of cadmium on cold and restraint stress-induced gastric lesions has been studied. Rats received 15 micrograms/mL cadmium-containing water for 30 d, and at the end of this period, they were subjected to cold and restraint stress. Cadmium accumulation in gastric mucosa was associated with increased mucosal lesions, as well as decreased mucin and PGE2 levels in rats exposed to cadmium. Stress-induced mucosal injury was more pronounced, and the hemoglobin leakage into gastric lumen owing to breakdown in the barrier was 17.30 +/- 3.45 micrograms/mL in control and 35.71 +/- 6.18 micrograms/mL in treated rats. Our data suggest that high cadmium intake facilitates the occurrence of stress-induced mucosal lesions by diminishing the mucin content and PGE2 generation in gastric mucosa.

Animals↗

PubMedDate not supplied

The effect of developmental exposure to cadmium (Cd) on visual evoked potentials (VEPs) and lipid peroxidation.

Pregnant Swiss albino rats were divided into three groups: control (C), gestational exposure of Cd (G-Cd), and gestational/postnatal exposure of Cd (GP-Cd) groups. Control animals received tap water, and the rats of GP-Cd group received Cd as CdC12 in their drinking water during the experimental period. The G-Cd group was given Cd during pregnancy, but given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be treated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an additional 38 days. On postnatal day (PND) 60, flash visual evoked potentials (FVEPs) were recorded with disc electrodes attached with collodion 0.5 cm in front of and behind bregma. The mean latencies on N1, P2, and P3 were prolonged in the GP-Cd group compared with controls. The mean latency of P3 was also significantly different between G-Cd and GP-Cd groups. P1-N1 and N1-P2 amplitudes of VEPs were significantly decreased in the GP-Cd group compared with control group. N1-P2 amplitude of the G-Cd group was significantly lower than that of the control group. Thiobarbituric acid reactive substances (TBARS) were determined as an indicator of lipid peroxidation. Our data showed that pre- and postnatal Cd treatment caused a significant increase of lipid peroxidation in the brain.

Analysis of Variance↗

PubMedDate not supplied

Cadmium induced lipid peroxidation in kidney function.

Since the kidney is the main target organ for many metals including cadmium, the generation of the products of lipid peroxidation due to accumulation of these toxic metals in the kidney may have importance in the mechanism of their nephrotoxicity. In order to test this hypothesis, we carried out an experimental study in rats. The functions and the levels of tiobarbituric acid reactive substances (TBARS) of the kidney were investigated in animals receiving 15 micrograms/ml aqueous Cd solution for 30 days. Due to cadmium accumulation in kidney cortex, the ratio of Cd/Zn increased significantly and this increase was associated with elevated TBARS in both renal cortex and medulla. The content of TBARS in renal cortex rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p<0.01) and GFR decreased to 390.5 +/- 109.4 from 1008.7 +/- 4.8 microliters/min (p<0.01) in cadmium exposed animals. Daily coadministration of selenium, vitamins A, C, E did not reverse the adverse effect of cadmium on kidney function, despite the significant decrease in cortex TBARS levels (p<0.01). In conclusion, these data suggest to us that lipid peroxidation assessed by TBA test may not be the only mechanism in cadmium induced nephrotoxicity.

Animals↗