Biomedical subjects

Tuncay Altug

Publications and source records attributed to Tuncay Altug.

7 recordsLinked to original sources

PubMed2005

The effects of tamoxifen on radiation-induced pulmonary fibrosis in Wistar albino rats: results of an experimental study.

This study was performed to evaluate the effects of tamoxifen on pulmonary fibrosis, given concurrently with or after irradiation in Wistar albino rats. Twenty-one female Wistar albino rats were randomized into three groups. The first group (Group A) had tamoxifen, which was started after the completion of irradiation. The second group (Group B) had tamoxifen concomitant with irradiation. The third group (Group C) had only thoracic irradiation and did not receive tamoxifen. Whole lungs were irradiated to a total dose of 30Gy in ten fractions with Co60. Tamoxifen was continued until the animals were sacrificed 16 weeks after the start of irradiation. As an end point the percentage of lung with fibrosis for each rat was quantified with image analysis of histological sections of the lung. Groups were compared using the one-way ANOVA method and Bonferroni post hoc test. The mean percentage values of fibrosis were 10.03 for Group A, 36.81 for Group B, and 3.87 for group C (P<0.001). When the percentages of fibrosis were compared for each group, the difference was statistically significant between Group A and Group B (P<0.001) and between Group B and Group C (P<0.001). Concomitant use of tamoxifen appears to increase radiation-induced pulmonary fibrosis and it seems more convenient to delay tamoxifen until the completion of irradiation.

Animals↗

PubMed2004

Spiral tacks may contribute to intra-abdominal adhesion formation.

PURPOSE: With the inception of laparoscopic ventral hernia repair came a novel device not used in conventional hernia repair; the spiral tack. We conducted an experimental study on pigs to determine whether spiral tacks contribute to adhesion formation. METHODS: Using a standard laparoscopic technique in pigs, pieces of polypropylene mesh were fixed to the fascia on the upper abdominal wall, with polypropylene sutures on a randomly chosen side (side 1), and with 5-mm spiral tacks on the opposite side (side 2). The extent, type, and tenacity of the adhesions were assessed on postoperative days (PODs) 30 and 90. RESULTS: The mesh fixed to the abdominal wall with spiral tacks tended to increase the extent, type, and tenacity of adhesions more than the mesh fixed with polypropylene sutures (P < 0.05). CONCLUSIONS: Spiral tacks contributed to the formation of adhesions more than polypropylene mesh did. Although this was a small-scale animal study, our findings suggest that the effect of spiral tacks used in laparoscopic ventral hernia repair should be assessed and the consequences monitored more closely.

Abdomen↗

PubMed2003

Green tea polyphenol (-)-epigallocatechin gallate prevents oxidative damage on periventricular white matter of infantile rats with hydrocephalus.

Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. Emphasizing the periventricular ischemia/hypoxia in hydrocephalus, various authors indicated the secondary biochemical impairment and oxidative damage in experimentally induced and congenital hydrocephalic rat brain. (-)-Epigallocatechin gallate (EGCG), the main constituent of green tea polyphenols, has been shown to be of some protective value in various models of neurological injury as a free oxygen radical scavenger. In the present study the effects of EGCG were examined on the periventricular oxidative damage in experimental childhood-onset hydrocephalus. Hydrocephalus was induced in 3 weeks-old rat pups by kaolin injection into the cisterna magna. A single daily dose of 50 mg/kg of EGCG injected into the peritoneum of the rats for 15 days significantly reduced periventricular white matter malondialdehyde levels when compared to non-treated hydrocephalic animals. Our results indicate that EGCG may have a protective effect against periventricular white matter oxidative damage in hydrocephalus induced infantile rats.

Animals↗

PubMed2002

Vitamin E supplementation in streptozotocin-treated rats alters cerebellar and plasma nitric oxide metabolism.

Nitric oxide (NO) free radicals appear to contribute to the pathogenesis of a number of disorders including diabetes mellitus. The aim of this study was to determine the effects of streptozotocin (STZ)-induced diabetes on nitric oxide (NO) metabolites in plasma and cerebellar nitric oxide synthase (NOS) activity. Further, it was of interest to determine whether an antioxidant, vitamin E, could reverse the STZ-induced effects. STZ significantly decreased cerebellar NOS but increased the level of plasma total nitrite + nitrate and the level of plasma nitrate. Supplementation with vitamin E effectively reduced the STZ-induced effects. Data demonstrate that vitamin E may serve as a protective antioxidant in STZ-induced diabetes.

Animals↗

PubMed2002

Curcumin's effects on sialic acid level and sialidase activity in Ehrlich ascites tumor bearing mice.

In this study, we determined curcumin's anticancer and chemopreventive effects in mice bearing Ehrlich ascites tumor by evaluation of cancer biomarkers, sialic acid level and sialidase activity. Both plasma sialic acid level and sialidase activity increased significantly in the mice group with Ehrlich ascites tumor. When the tumor groups fed with curcumin and fed with sesame oil were compared, sialic acid level and sialidase activity in ascites fluid significantly reduced in the group fed with curcumin in addition to the increases of plasma sialic acid level and sialidase activity. The tumor group fed with curcumin lived twice longer than the one fed with sesame oil. Curcumin as a phenolic compound decreased all these parameters in Ehrlich ascites tumors and lengthened survival by 88% in the mice with tumor. We concluded that curcumin has anticancer activity.

Animals↗

PubMed2002

N-acetylcysteine reduced the effect of ethanol on antioxidant system in rat plasma and brain tissue.

Chronic ethanol administration is able to induce an oxidative stress in the central nervous system. N-Acetylcysteine (NAC) has antioxidant properties; as a sulphydryl donor, it contributes to the regeneration of glutathione and it acts through a direct reaction with hydroxyl radicals. In this study we investigated a possible beneficial effect of NAC on some of the free radical related parameters. Twenty four male Wistar rats were divided in to three groups and were given ethanol (Group 1), ethanol and NAC (Group 2) and isocaloric dextrose (Group 3). Ethanol and NAC were given intragastrically at doses of 6 g/kg/day and 1 g/kg/day, respectively. Our results show that chronic ethanol intake elicits statistically significant increase in MDA and NO levels and decrease in SOD and GSH levels in both plasma and brain (p < 0.001). GPx levels decreased in erythrocytes (p < 0.001). CAT activity showed significant decrease only in brain samples (p < 0.001). NAC administration effectively restores the above results to nearly normal levels. Therefore we suggest that reactive free radicals are, at least partly, involved in the ethanol-induced injury of brain cells and NAC mitigate the toxic effects of ethanol on the oxidant-antioxidant system of rat plasma and brain.

Acetylcysteine↗

PubMedDate not supplied

Decrease in mitochondrial oxidative protein damage parameters in the streptozotocin-diabetic rat.

BACKGROUND: Many authors have shown that hyperglycemia leads to an increase in oxidative protein damage in diabetes. The aim of this study was to reveal the susceptibility of mitochondria from liver, pancreas, kidney, and skeletal muscle of diabetic Sprague-Dawley rats, a model of type 1 diabetes, to oxidative protein damage. METHODS: Mitochondrial fractions were obtained by differential centrifugation. To show the effect of hyperglycemia in promoting oxidative protein damage, we determined mitochondrial protein carbonyl, total thiol, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels. The levels of the studied markers, except nitrotyrosine, were determined by colorimetric methods. Nitrotyrosine levels were measured by ELISA. All values were compared with those of the controls by using the Mann-Whitney U-test. RESULTS: Nitrotyrosine and lipid hydroperoxide levels were decreased and other parameters were not changed in liver mitochondria of diabetic rats. Protein carbonyl, nitrotyrosine, advanced oxidation protein products, and lipid hydroperoxide levels were decreased and total thiol levels were not changed in pancreas mitochondria of diabetic rats. Only advanced oxidation protein products and lipid hydroperoxide levels were decreased in kidney mitochondria of diabetic rats. The levels of the same parameters were not significantly different in muscle mitochondria of diabetic rats. CONCLUSIONS: The decrease in mitochondrial oxidative protein damage in diabetes may correspond to either an increase in antioxidant defense mechanisms or a different adaptive response of the cells to the increased extramitochondrial oxidative stress in diabetes. The mitochondrial oxidative protein damage-lowering mechanisms in diabetes remain to be clarified.

Animals↗