Carani Venkatraman Anuradha

Gastroprotective effect of fenugreek seeds (Trigonella foenum graecum) on experimental gastric ulcer in rats.

The effect of fenugreek seeds (Trigonella foenum graecum) compared to omeprazole was studied on ethanol-induced gastric ulcer. The aqueous extract and a gel fraction isolated from the seeds showed significant ulcer protective effects. The cytoprotective effect of the seeds seemed to be not only due to the anti-secretory action but also to the effects on mucosal glycoproteins. The fenugreek seeds also prevented the rise in lipid peroxidation induced by ethanol presumably by enhancing antioxidant potential of the gastric mucosa thereby lowering mucosal injury. Histological studies revealed that the soluble gel fraction derived from the seeds was more effective than omeprazole in preventing lesion formation. These observations show that fenugreek seeds possess antiulcer potential.

EXERCISE, DEPLETION OF ANTIOXIDANTS AND ANTIOXIDANT MANIPULATION

Strenuous physical activity is known to increase the production of reactive oxygen species (ROS), associated with depletion of antioxidant defence. In the present work we evaluated the level of lipid peroxidation and antioxidant components in blood of sportsmen under resting conditions and compared the data obtained with those in age‐ and sex‐matched sedentary controls. A significant increase was noted in the levels of thiobarbituric acid reactive substances (TBARS) and conjugated dienes while a decrease was observed in ascorbic acid and glutathione levels in sportsmen. α‐Tocopherol was unaltered in plasma of sportsmen as compared to controls. The activity of superoxide dismutase was increased (52 per cent) and glutathione peroxidase was decreased (43 per cent) in the erythrocytes of sportsmen compared to controls. Basal glutathione levels were negatively correlated with conjugated dienes and maximal oxygen uptake (VO2max) of the subjects. Dietary supplementation with antioxidant vitamins has been shown to be beneficial in combating oxidative stress without enhancing performance while exogenous glutathione was found to influence the endurance capacity of athletes. Such studies demonstrate the critical role played by glutathione and suggest that intervention trials should include a mixture of antioxidants rather than a single antioxidant. Copyright

Investigation of antioxidant, anti-inflammatory and DNA-protective properties of eugenol in thioacetamide-induced liver injury in rats.

The present study investigated the preventive effect of eugenol, a naturally occurring food flavouring agent on thioacetamide (TA)-induced hepatic injury in rats. Adult male Wistar rats of body weight 150-180 g were used for the study. Eugenol (10.7 mg/kg b.w./day) was administered to rats by oral intubation for 15 days. TA was administered (300 mg/kg b.w., i.p.) for the last 2 days at 24h interval and the rats were sacrificed on the 16th day. Markers of liver injury (aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma-glutamyl transferase and bilirubin), inflammation (myeloperoxidase, tumor necrosis factor-alpha and interleukin-6), oxidative stress (lipid peroxidation indices, protein carbonyl and antioxidant status) and cytochrome P4502E1 activity were assessed. Expression of cyclooxygenase-2 (COX-2) and the extent of DNA damage were analyzed using immunoblotting and comet assay, respectively. Liver injury and collagen accumulation were assessed using histological studies by hematoxylin and eosin and Masson trichrome staining. Rats exposed to TA alone showed increased activities of hepatocellular enzymes in plasma, lipid peroxidation indices, inflammatory markers and pro-inflammatory cytokines and decreased antioxidant status in circulation and liver. Hepatic injury and necrosis were also evidenced by histology. Eugenol pretreatment prevented liver injury by decreasing CYP2E1 activity, lipid peroxidation indices, protein oxidation and inflammatory markers and by improving the antioxidant status. Single-cell gel electrophoresis revealed that eugenol pretreatment prevented DNA strand break induced by TA. Increased expression of COX-2 gene induced by TA was also abolished by eugenol. These findings suggest that eugenol curtails the toxic effects of TA in liver.

Effect of fenugreek seeds on blood lipid peroxidation and antioxidants in diabetic rats.

The effect of fenugreek seeds (Trigonella foenum graecum) on blood lipid peroxidation and antioxidant status in alloxan diabetic rats was studied. Increased lipid peroxidation and alterations in circulating antioxidants were observed in the diabetic state. The levels of glutathione, ascorbic acid and β‐carotene in blood were significantly lowered and α‐tocopherol content was increased. Supplementation of fenugreek seeds in the diet lowered lipid peroxidation. The contents of glutathione and β‐carotene were increased and the α‐tocopherol content was lowered. The level of ascorbic acid was unaltered. The level of antioxidants were higher in normal rats which were fed with the fenugreek supplemented diet compared with control animals which were fed commercial rat chow. The study shows that disrupted free radical metabolism in diabetic animals may be normalized by fenugreek seed supplementation in the diet.Copyright

Taurine restores ethanol-induced depletion of antioxidants and attenuates oxidative stress in rat tissues

Summary.Ethanol by its property of generating free radicals during the course of its metabolism causes damage to cell structure and function. The study investigates the protective effects of the antioxidant aminoacid taurine on ethanol-induced lipid peroxidation and antioxidant status. Male Wistar rats of body weight 170–190 g were divided into 4 groups and maintained for 28 days as follows: a control group and taurine-supplemented control group, taurine supplemented and unsupplemented ethanol-fed group. Ethanol was administered to rats at a dosage of 3 g/kg body weight twice daily and taurine was provided in the diet (10 g/kg diet). Lipid peroxidation products and antioxidant potential were quantitated in plasma and in following tissues liver, brain, kidney and heart.Increased levels of thiobarbituric acid substances (TBARS) and lipid hydroperoxides (LHP) in plasma and tissues, decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were observed in hemolysate and tissues of ethanol-fed rats. The contents of reduced glutathione (GSH), α-tocopherol and ascorbic acid in plasma and tissues were significantly reduced in these animals as compared to control animals. Simultaneous administration of taurine along with ethanol attenuated the lipid peroxidation process and restored the levels of enzymatic and non-enzymatic antioxidants. We propose that taurine may have a bioprotective effect on ethanol-induced oxidative stress.

Effect of L-Carnitine on Skeletal Muscle Lipids and Oxidative Stress in Rats Fed High-Fructose Diet

There is evidence that high-fructose diet induces insulin resistance, alterations in lipid metabolism, and oxidative stress in rat tissues. The purpose of this study was to evaluate the effect of L-carnitine (CAR) on lipid accumulation and peroxidative damage in skeletal muscle of rats fed high-fructose diet. Fructose-fed animals (60 g/100 g diet) displayed decreased glucose/insulin (G/I) ratio and insulin sensitivity index (ISI0,120) indicating the development of insulin resistance. Rats showed alterations in the levels of triglycerides, free fatty acids, cholesterol, and phospholipids in skeletal muscle. The condition was associated with oxidative stress as evidenced by the accumulation of lipid peroxidation products, protein carbonyls, and aldehydes along with depletion of both enzymic and nonenzymic antioxidants. Simultaneous intraperitoneal administration of CAR (300 mg/kg/day) to fructose-fed rats alleviated the effects of fructose. These rats showed near-normal levels of the parameters studied. The effects of CAR in this model suggest that CAR supplementation may have some benefits in patients suffering from insulin resistance.

Influence of alpha-lipoic acid on lipid peroxidation and antioxidant defence system in blood of insulin-resistant rats.

Background:  High fructose feeding induces insulin resistance and hyperinsulinaemia in rats. A role for oxidative stress in the occurrence of insulin resistance has been suggested by several workers.

Taurine modifies insulin signaling enzymes in the fructose-fed insulin resistant rats.

OBJECTIVES High fructose feeding induces insulin resistance and hyperinsulinemia in rats. The present study was proposed to elucidate the derangements in the insulin signaling pathway in high fructose-fed rats and whether taurine, a sulphur-containing amino acid could improve insulin action by modulating the signal transduction pathway. METHODS Male Wistar rats of body weight 170-190 g were divided into 4 groups of 6 rats each. Control rats received control diet and water ad libitum. Fructose fed animals received high fructose diet (> 60% of total calories) and water ad libitum. Fructose + taurine rats received fructose diet and 2% taurine solution ad libitum. Control + taurine rats received control diet and 2% taurine solution ad libitum. After the experimental period of 30 days, the effects of taurine on certain parameters on glucose metabolism were determined. The activities of protein tyrosine kinase (PTK) and protein tyrosine phosphatase (PTP) were assayed in liver. RESULTS The activities of the glycolytic enzymes were significantly lower while the activities of the gluconeogenic enzymes were higher in untreated fructose-fed rats as compared to control animals. Depletion of liver glycogen was observed in fructose-fed rats. Fructose-fed rats showed alterations in the activities of insulin signaling enzymes PTK and PTP. Taurine administration improved insulin sensitivity and controlled hyperglycemia and hyperinsulinemia in fructose-fed rats. Taurine treatment also restored the glucose metabolizing enzyme activities in fructose-fed rats. CONCLUSIONS Taurine supplementation might have a beneficial effect in overcoming insulin resistance and its associated abnormalities by modifying the post-receptor events of insulin action.

Metformin improves lipid metabolism and attenuates lipid peroxidation in high fructose-fed rats

Aim: Insulin resistance, hyperinsulinaemia and disturbances in glucose metabolism can be produced in normal rats by feeding them a fructose‐enriched diet. Metformin, an antidiabetic drug, enhances insulin sensitivity in type 2 diabetic patients. Previous studies have shown that metformin improves insulin sensitivity in fructose‐fed rats. The aim of this study was to determine the effect of metformin treatment on overall lipid metabolism and lipid peroxidation in rats that were fed a fructose‐enriched diet, which leads to insulin resistance. The relationship between hyperinsulinaemia and hyperglycaemia with lipid peroxide levels was also investigated.

Suppression of hepatic oxidative events and regulation of eNOS expression in the liver by naringenin in fructose-administered rats.

Previous studies show that naringenin promotes insulin sensitivity in fructose-fed rats. This study investigates whether naringenin prevents oxidative events and apoptotic changes triggered in the rat liver by a high fructose diet. Male Wistar rats of body weight 150-180 g were fed either diet containing starch (60% carbohydrate) or fructose (60% fructose diet). From the 16th day of feeding, rats in each dietary group were divided into two, and treated or not with naringenin (50mg/kg b.w/day). After 60 days, oxidative and nitrosative damage and endothelial nitric oxide synthase (eNOS) expression and hepatocyte apoptosis were determined. To evaluate whether nitric oxide (NO) plays a role in naringenin action, insulin sensitivity indices, fasting plasma glucose and insulin were assessed in response to co-administration of L-nitro-arginine methyl ester (L-NAME), a NOS inhibitor. Fructose feeding caused oxidative damage to proteins and lipids and resulted in reduced antioxidant status, eNOS expression and nitrite level. Increased formation of 4-hydroxy nonenal (4-HNE), 2, 4-dinitrophenol (2, 4-DNP) and 3-nitrotyrosine (3-NT)-modified proteins and the presence of apoptotic nuclei were observed in the liver. Treatment with naringenin attenuated all these parameters to levels not significantly different from control. Treatment with naringenin improved insulin sensitivity. However, L-NAME plus naringenin administration abolished the insulin-sensitizing effects of naringenin in fructose-fed rats. Reduced oxidative events with simultaneous increase in NO bioavailability may be involved in the insulin-sensitizing and cytoprotective effects of naringenin in fructose-fed rats.