Gül Özdemirler

Effect of pretreatment with artichoke extract on carbon tetrachloride-induced liver injury and oxidative stress

Artichoke is a plant with antioxidant properties. In this study, we investigated the effect of artichoke extract pretreatment on carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity. Rats were given artichoke leaf extract (1.5g/kg/day) by gavage for 2 weeks and after then CCl4 (1ml/kg; i.p.) was applied. All rats were killed 24h after the CCl4 injection. CCl4 administration resulted in hepatic necrosis and significant increases in plasma transaminase activities as well as hepatic malondialdehyde (MDA) and diene conjugate (DC) levels in the liver of rats. Glutathione (GSH) and vitamin C levels decreased, but vitamin E levels increased in the liver of CCl4-treated rats. Hepatic superoxide dismutase (SOD) activities remained unchanged, but glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities decreased following CCl4 treatment. In rats pretreated with artichoke extract, significant decreases in plasma transaminase activities and amelioration in histopathological changes in the liver were observed following CCl4 treatment as compared to CCl4-treated rats. In addition, hepatic MDA and DC levels decreased, but GSH levels and GSH-Px activities increased without any change in other antioxidant parameters following CCl4 treatment in artichoke-pretreated rats. The present findings indicate that in vivo architoke extract administration may be useful for the prevention of oxidative stress-induced hepatotoxicity.

Ethanol-induced changes in lipid peroxidation and glutathione content in rat brain

The effect of acute and chronic ethanol administration on brain lipid peroxide and glutathione levels was investigated in rats. Acute ethanol administration (5 g/kg, i.p.) led to an increase in lipid peroxide levels and a decrease in glutathione levels in whole brain homogenates without cerebellum. However, there was no change in brain lipid peroxide and glutathione levels of rats chronically treated with ethanol.

Role of carnosine in preventing thioacetamide-induced liver injury in the rat

Carnosine (beta-alanyl-L-histidine) is a dipeptide with antioxidant properties. Free radicals are involved in the pathogenesis of acute liver injury induced by thioacetamide (TAA). In this study, we investigated the effect of carnosine treatment on TAA-induced oxidative stress and hepatotoxicity. Rats were injected intraperitoneally with TAA (500 mg/kg) and carnosine (250 mg/kg, intraperitoneal) was co-administered with TAA. All animals were killed 24 h after injections. TAA administration resulted in hepatic necrosis, significant increases in plasma transaminase activities as well as hepatic lipid peroxide levels. In addition, hepatic antioxidant system was found to be depressed following TAA administration. When carnosine was co-administered with TAA in rats, plasma transaminase activities were found to approach to normal values in rats. Histological findings also suggested that carnosine has preventive effect on TAA-induced hepatic necrosis. Carnosine treatment caused significant decreases in lipid peroxide levels in TAA-treated rats without any changes in enzymatic and non-enzymatic antioxidants except vitamin E in the liver of rats. Our findings indicate that carnosine, in vivo may have a preventive effect on TAA-induced oxidative stress and hepatotoxicity by acting as an non-enzymatic antioxidant itself.

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.

Mitochondrial Lipid Peroxides and Antioxidant Enzymes in Colorectal Adenocarcinoma Tissues

Lipid peroxide levels and superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and glutathione transferase (GST) activities were investigated in mitochondrial fractions obtained from tumorous and nontumorous colorectal tissues of fourteen patients with colon and rectum cancer. Histopathological evaluations, including type, stage, necrosis and lymphocyte infiltration were also performed for each patient. The activities of SOD, GSH‐Px and GST were increased significantly, but lipid peroxide levels remained unchanged in mitochondria obtained from tumors compared to adjacent normal tissues of subjects with colorectal cancer. When the patients were grouped according to their histopathological evaluation, such as type, stage, necrosis and lymphocyte infiltration, no relationship was observed between the histopathological results and the mitochondrial lipid peroxidation or antioxidant enzyme activities.

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 hepatic lipid peroxidation, copper and fibrosis in cholestatic rats.

Hepatic lipid peroxidation was shown to be stimulated in the livers of cholestatic rats with increased hydroxyproline levels. In another group, cholestatic rats were fed with a copper-supplemented diet to increase hepatic copper levels. Although liver copper concentrations increased about 16-fold in copper supplemented cholestatic rats compared to normally fed cholestatic rats, no change was observed either in hepatic lipid peroxidation or in hydroxyproline levels.

Inhibition of NADPH-induced microsomal lipid peroxidation in the livers of cholestatic rats

NADPH-induced microsomal lipid peroxidation was found to be significantly inhibited in the livers of cholestatic rats. In cholestasis, microsomal cholesterol content was increased while phospholipid content remained unchanged.