Gülçin Toker

High cholesterol diet supplemented with sunflower seed oil but not olive oil stimulates lipid peroxidation in plasma, liver, and aorta of rats

Abstract To determine the effect of a high cholesterol diet supplemented with sunflower seed oil or olive oil on plasma, liver, and aorta lipid peroxidation, rats were fed a basal diet, a high cholesterol diet (basal diet containing 2% cholesterol and 0.5% cholic acid), or a high cholesterol diet supplemented with 10% ( wt wt ) sunflower seed oil or 10% ( wt wt ) olive oil for 4 months. In rats fed the high cholesterol diet supplemented with sunflower seed oil, plasma, liver, and aorta lipid peroxide levels and the aorta cholesterol to phospholipid ratio were greater than in rats fed the high cholesterol diet. In contrast, no change was observed in plasma, liver, and aorta lipid peroxidation and the cholesterol to phospholipid ratio in rats fed the high cholesterol diet containing olive oil as compared with the high cholesterol diet. In addition, atherosclerotic lesions were not detected in the aorta of all groups. We concluded that a high cholesterol diet supplemented with polyunsaturated fats, but not with monounsaturated fats, seems to have a tendency to exaggerate lipid peroxidation.

Increased lipoperoxide levels and antioxidant system in colorectal cancer

Abstract In this study, lipid peroxide and glutathione (GSH) levels, GSH peroxidase, GSH S-transferase, superoxide dismutase, γ-glutamylcysteine synthetase and γ-glutamyl transpeptidase activities were investigated in tumorous and nontumorous colorectal tissues obtained from ten patients diagnosed with colon and rectum cancer. Histopathological evaluations, including type, stage, necrosis and lymphocyte infiltration, were also performed for each patient. According to the results, lipid peroxide and GSH levels and the activities of GSH peroxidase, superoxide dismutase, γ-glutamylcysteine synthetase were found to be increased, while GSH S-transferase and γ-glutamyl transpeptidase activities remained unchanged in tumors compared to adjacent normal tissues of subjects with colorectal cancer. However, the considerable interindividual variations were found in these parameters. A definite interrelation between histopathological results with lipid peroxidation and antioxidant system was not observed.

The Effect of Melatonin on TNBS-Induced Colitis

Ulcerative colitis is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. The present study was undertaken to investigate the effect of melatonin administration on oxidative damage and apoptosis in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Rats were divided into four groups as follows: Group 1 (n=8)—TNBS colitis; Group 2 (n=8)—melatonin, 10 mg/kg/day ip, for 15 days in addition to TNBS; Group 3 (n=8)—melatonin alone, 10 mg/kg/day ip, for 15 days; and Group 4 (n=8)—isotonic saline solution, 1ml/rat ip, for 15 days (sham control group). Colonic myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels, and glutathione (GSH) levels are indicators of oxidative damage, while caspase-3 activities reveal the degree of apoptosis of the colonic tissue. In all TNBS-treated rats, colonic MPO activity and MDA levels were found to be increased significantly compared to those in the sham group. Colonic MPO activity and MDA levels were significantly lower in the melatonin treatment group compared to TNBS-treated rats. GSH levels of colonic tissues were found to be significantly lower in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly increased GSH levels compared to those in TNBS-treated rats. Caspas-3 activity of colonic tissues was found to be significantly higher in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly decreased caspase-3 activity compared to that in TNBS-treated rats. These results imply a reduction in mucosal damage due to anti-inflammatory and anti-apoptotic effects of melatonin.

Nitric oxide and radiation enteritis.

OBJECTIVE To investigate the changes in intestinal nitric oxide (NO) and myeloperoxidase (MPO) concentrations, the rate of endotoxaemia, and intestinal mucosal structure in rats after irradiation of the abdomen and to find out the effect of Nomega-nitroarginine methyl ester (L-NAME) inhibition NO synthesis. SETTING Medical school, Turkey. DESIGN Experimental study. MATERIAL 46 Wistar-albino rats. INTERVENTIONS In Group I (n = 12), rats underwent abdominal irradiation alone. In Group II (n = 12), they underwent abdominal irradiation and were given L-NAME orally for 3 days before and 3 days after irradiation. In Group III (n = 12), rats had abdominal irradiation and were given L-NAME orally for 3 days after irradiation. Group IV (n = 10) were controls and were untreated. The irradiation procedure consisted of a single shot of 1000 cGy to the abdomen and L-NAME was given 30 mg/kg/day orally in the drinking water. MAIN OUTCOME MEASURES Intestinal mucosal MPO and nitrite, and plasma endotoxin concentrations. Changes in villous height and number were recorded. RESULTS In groups II and III, MPO and NO2- concentrations decreased significantly compared with group I. Mucosal integrity was protected in both groups treated with L-NAME (groups II and III) in contrast to the group given irradiation without treatment (group I). CONCLUSION These results suggest that the NO pathway contributes to the inflammatory response of radiation enteritis. Inhibition of NO synthesis may have a beneficial effect in the treatment of inflammation caused by irradiation.

The effect of heme oxygenase-1 induction by octreotide on radiation enteritis

Radiation enteritis occurs as a response to abdominal radiation, which can cause mucosal damage in the gastrointestinal mucosal epithelium. The small intestine is one of the most radiosensitive organs in the abdomen. The present study was undertaken to investigate the effect of octreotide (OCT) administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. Rats received 50 mg/kg/day OCT for 4 days before irradiation and continued for 3 days after irradiation. Intestinal myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels are indicators of oxidative damage while caspase-3 activities reveal apoptosis degree of the small intestine. At histological examination, the terminal ileum tissue was analyzed for morphological changes. Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels and HO-1 expression in comparison to sham control group. OCT treatment was associated with increased HO-1 expression and caspase-3 activity, decreased MPO activity and MDA levels. Histological examination revealed that the intestinal mucosal structure was preserved in the OCT treated group. OCT appears to have protective effects against radiation-induced intestinal damage. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO-1 expression.

The Efficacy of Octreotide in Pancreatic and Intestinal Changes: Radiation-Induced Enteritis in Animals

Radiation enteritis occurs during the radiotherapy of many intraabdominal malignancies. Radiation induces cellular injury directly and through the generation of free radicals. In the present study we aimed to investigate the effect of octreotide (OCT) pretreatment in irradiation-induced enteritis. For this aim, rats were injected with 50 μg/kg OCT 4 days before irradiation and continued for 3 more days, until sacrifice. Then intestinal and pancreatic myeloperoxidase (MPO) activities and intestinal malondialdehyde (MDA) levels of the rats were measured. Irradiation significantly increased intestinal and pancreatic MPO activities and MDA levels of intestinal tissues in comparison to those of the sham group. OCT treatment improved this elevation. The histopathologic evaluation of the mucosal structure was also preserved in the OCT-treated group. Inflammation of pancreatic tissue was also confirmed with histopathological examinations. In the irradiation group, NFκ-B overexpression was detected. OCT treatment decreased the end organ damage and inflammation of the small intestine. In conclusion, OCT appears to have beneficial effects on intestinal and pancreatic damage in abdominal irradiation through the inflammatory process.

Effect of heme oxygenase‐1 induction by octreotide on TNBS‐induced colitis

Background and Aim:  Ulcerative colitis is a chronic inflammatory disease of the colon and rectum. Although the precise etiology of ulcerative colitis remains unknown, it is believed to involve an abnormal host response to endogenous or environmental antigens, genetic factors, and oxidative damage. The aim of the present study was to investigate whether heme oxygenase‐1 (HO‐1) induction by octreotide could protect against oxidative and inflammatory damage from induced colitis.

Age-related changes in plasma lipid peroxidation and antioxidant system in humans and rats.

This study was carried out on young (20-35 years) and old (60-85 years) men and rats (6 vs 22 months) to investigate the effect of aging on plasma lipid peroxidation and the antioxidant system. Plasma polyunsaturated fatty acid (PUFA), total fatty acid (TFA) and malondialdehyde (MDA) levels increased in aged humans and rats compared with young groups. However, plasma MDA/TFA ratios did not increase in aged humans and rats. Plasma vitamin E/TFA, and total thiol content were found to decrease both in aged humans and rats. Plasma antioxidant activity (AOA) decreased only in aged rats. In addition, the susceptibility of VLDL+LDL, apolipoprotein B containing lipoproteins to copper-induced peroxidation increased with aging. It is concluded that aging is associated with some variations in plasma oxidant-antioxidant balance.

The Effect of Octreotide on Pancreatic Damage in TNBS-Induced Colitis

Inflammatory bowel disease, a chronic condition of the intestine, is associated with numerous extraintestinal manifestations, including pancreatitis. This study investigated the effect of octreotide administration on oxidative damage in a rat model of colitis induced by 2,4,6-trini-trobenzene sulfonic (TNBS) acid. Colonic and pancreatic malondialdehyde and glutathione levels are indicators of oxidative damage, and TNBS-induced colitis significantly increased the colonic and pancreatic malondialdehyde levels and decreased glutathione levels. Octreotide treatment was associated with decreased malondialdehyde levels and increased glutathione levels in the colonic and pancreatic tissue. The colonic mucosal structure was preserved and pancreatic inflammation decreased in rats treated with octreotide. Octreotide also significantly decreased nuclear factor-kB expression by immunohisto-chemistry in the colonic and pancreatic tissue compared with TNBS-induced colitis group. Octreotide appears to have protective effects against TNBS-induced colonic and pancreatic damage. These results imply the reduction in mucosal damage owing to the anti-inflammatory and antioxidant effects of octreotide.