Protective role of ferulic acid on carbon tetrachloride-induced hyperlipidemia and histological alterations in experimental rats.

BACKGROUND: The present study aimed to evaluate the antihyperlipidemic effect of ferulic acid (FA) on carbon tetrachloride (CCl4)-treated rats. METHODS: Female albino rats of the Wistar strain were used in the present study. The rats were divided into four groups: groups 1 and 4 received physiological saline (3 mL/kg body weight/week) by subcutaneous injection, whereas groups 2 and 3 received a subcutaneous injection of CCl4 (3 mL/kg body weight/week) for a total period of 12 weeks. In addition, groups 3 and 4 were administered FA (20 mL/kg body weight) every day for the last 90 days. RESULTS: The results showed significantly (p≤0.05) elevated levels of cholesterol, triglycerides (TG), and free fatty acids (FFA) in the liver and kidney of CCl4-treated rats as compared with those of the controls. In addition, the levels of cholesterol, FFA, phospholipids (PL), and TG were elevated significantly in the circulation. Administration of FA effectively reduced these levels of lipids in the plasma, liver, and kidney of CCl4-treated rats. The PL level was significantly decreased in the liver and kidney of CCl4-treated rats and was positively modulated by FA treatment. Our histopathological observations were also in correlation with the biochemical parameters. CONCLUSIONS: From the results obtained, we could conclude that FA effectively protects the system against hyperlipidemia and may be an effective therapeutic agent for the treatment of this disorder.

Antihyperlipidemic effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione, a curcumin analog, on nicotine and streptozotocin treated rats.

Diabetes and smoking have been considered as major health problems individually and their seriousness related to health hazard has been well reported. Data regarding the possible contribution of cigarette smoking to the development of diabetes are scarce and inconclusive. The aim was to investigate the effect of nicotine on diabetes and to analyze the effect of bis demethoxy curcumin analog (BDMCA) in streptozotocin (STZ) and nicotine-induced toxicity. The tissue lipids were extracted according to the method of Folch et al. Plasma and tissue cholesterol was estimated by the method of Allain et al. using reagent kit. Triglycerides were estimated by the method of Foster and Dunn. Free fatty acids were estimated by the method of Falholt et al. Tissue phospholipids were estimated by the method of Zilversmit and Davis. From our study, we found that nicotine not only aggravates diabetic complications but also increased the risk for diabetes. BDMCA, at a dose 80 mg/kg body weight was found to be effective in decreasing toxic effects induced by nicotine and STZ. Our data provide new evidence that cigarette smoking is an additional important factor that could be targeted for the prevention of diabetic complications.

Prevention of nicotine and streptozotocin treatment induced circulatory oxidative stress by bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione in diabetic rats.

Diabetes and smoking have been considered as major health problems individually and their seriousness related to health hazard has been well reported. The role of nicotine in causing or worsening effect on diabetes is not well understood. The aim of our study was to investigate the effect of nicotine on experimental diabetes and to analyze the effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione a bisdemethoxy curcumin analog (BDMCA) in streptozotocin and nicotine induced toxicity. Group I: control rats; Group II: nicotine (2.5 mg/kg b.wt); Group III: streptozotocin (STZ) (40 mg/kg b.wt); Group IV: STZ (40 mg/kg b.wt) + nicotine (2.5 mg/kg b.wt); Group V: STZ + nicotine + BDMCA (40 mg/kg b.wt); Group VI: STZ + nicotine + BDMCA (80 mg/kg b.wt). Efficacy of BDMCA was determined by evaluating blood glucose, thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP), activities of marker enzymes alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) and activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). From our study, we have observed that nicotine not only aggravates diabetic complications but also increased the risk for diabetes. BDMCA, at a dose 80 mg/kg body weight was found to be more effective in decreasing toxic effects induced by nicotine and STZ.

Suppression of constitutively expressed cyclooxygenase-2 in the epididymis of mice by nimesulide decreases sperm motility.

Significant levels of constitutive cyclooxygenase-2 (COX-2) are present in the male reproductive organs of rodents, especially in the vas deferens and epididymis. In the epididymis, the sperm storehouse, COX-2 is thought to play a vital role in altering the membrane lipids of sperm. The present study aims at localizing COX-2 in the epididymis and analyzing the effects of the preferential COX-2 inhibitor nimesulide. COX-2 protein activity was nearly equal to that of COX-1 in the cauda epididymis. Immunohistochemical studies showed an intense staining for COX-2 in the cauda epididymis but not in the caput epididymis. Nimesulide administration induced a significant reduction in both COX-2 staining intensity and protein activity, followed by an initial decline in total prostaglandin levels but a reversible increase upon sustained COX-2 suppression. Sperm numbers and vitality showed no significant change, but motility decreased and total and free serum testosterone levels mildly increased.

Effect of quercetin on nicotine-induced biochemical changes and DNA damage in rat peripheral blood lymphocytes.

We elucidated the protective effect of quercetin, a polyphenolic flavonoid, on lipid peroxidation, endogenous antioxidant status and DNA damage during nicotine-induced toxicity in cultured rat peripheral blood lymphocytes as compared to N-acetylcysteine (NAC), a well-known antioxidant. Lymphocytes were exposed to nicotine (3 mM) with and without quercetin and NAC (1 mM) in RPMI-1640 medium for 1 h. In preliminary experiments to fix the effective dose of quercetin, different doses of quercetin (25, 50, 75, 100 and 200 microM) were administered to lymphocytes with nicotine, and lipid peroxidation markers (thiobarbituric acid reactive substances and hydroperoxides) were analysed. A 75 microM dose of quercetin was found to be effective as evidenced by decreased lipid peroxidation. To evaluate the protective potential of quercetin against genotoxic effects of nicotine we used comet and micronucleus assays, which are valid parameters to assess genetic damage. In addition, biochemical changes including lipid peroxidation and antioxidant status were assessed. There were significant increases in the levels of lipid peroxidation, comet parameters and micronuclei frequencies, followed by decrease in the endogenous antioxidant status, in nicotine-treated lymphocytes, which were brought back to near normal by quercetin or NAC treatment. The protective effect of quercetin against nicotine toxicity was comparable to that of NAC. These findings suggest that quercetin can be as effective as NAC in protecting rat peripheral lymphocytes against nicotine-induced cellular and DNA damage.

Modulatory potential of ellagic acid, a natural plant polyphenol on altered lipid profile and lipid peroxidation status during alcohol-induced toxicity: a pathohistological study.

Polyphenol-rich dietary foodstuffs, consumed as an integral part of vegetables, fruits, and beverages have attracted attention due to their antioxidant and anticancer properties. Ellagic acid (EA), a polyphenolic compound widely distributed in fruits and nuts, has been reported to scavenge free radicals and inhibit lipid peroxidation. Chronic consumption of alcohol potentially results in serious illness including hepatitis, fatty liver, hypertriglyceridemia, and cirrhosis. A little is known about the influence of EA on alcohol toxicity in vivo. Accordingly, in the present study, we have evaluated the protective effects of EA on lipid peroxidation and lipid levels during alcohol-induced toxicity in experimental rats. Forty female albino Wistar rats, which were weighing between 150-170 g were used for the study. The toxicity was induced by administration of 20% alcohol orally (7.9 g/kg body wt.) for 45 days. Rats were treated with EA at three different doses (30, 60, and 90 mg/kg body wt.) via intragastric intubations together with alcohol. At the end of experimental duration, liver marker enzymes (i.e., aspartate transaminase, alanine transaminase), lipid peroxidative indices (i.e., thiobarbituriacid reactive substances and hydroperoxides) in plasma, and lipid levels (i.e., cholesterol, free fatty acids, triglycerides and phospholipids) in tissues were analyzed to evaluate the antiperoxidative and antilipidemic effects of EA. Liver marker enzymes, lipid peroxidative indices, and lipid levels, i.e., cholesterol, triglycerides and free fatty acids, were significantly increased whereas phospholipid levels were significantly decreased in the alcohol-administered group. EA treatment resulted in positive modulation of marker enzymes, peroxidative indices, and lipid levels. EA at the dose of 60 mg/kg body wt. was found to be more effective when compared to the other two doses. Histological changes observed were also inconsistent with the biochemical parameters. Our study suggests that EA exerts beneficial effects at the dosage of 60 mg/kg body wt. against alcohol-induced damage, and it can be used as a potential drug for the treatment of alcohol-abuse ailments in the near future.

Localization of cyclooxygenase-2 in mice vas deferens and its effects on fertility upon suppression using nimesulide: a preferential cyclooxygenase-2 inhibitor.

Accumulating evidence on constitutive expression of cyclooxygenase-2 (COX-2), one of the isoforms of enzyme cyclooxygenase (COX) the other isoform being cyclooxygenase-1 (COX-1), questions the safety profile of non-steroidal anti-inflammatory drugs (NSAIDs). This COX-2 isoform which is induced not only during inflammation but also by factors such as cytokines, steroid hormones and mitogenic stimuli is constitutively expressed in brain, kidney and reproductive organs. Present NSAIDs, particularly COX-2 inhibitors is no longer considered safe since suppression of COX-2 in tissues which it is constitutively expressed may lead to adverse effects. Though intense expression of COX-2 in vas deferens is proved, lack of information with respect to its function has attracted a wide scope for research as to whether COX-2 in vas deferens contributes to male fertility. In the present study, the authors investigated the localization of COX-2 as well as COX-1 in mice vas deferens and also assessed the activity of COX-2 and total prostaglandin (PG) levels in vas deferens. Further they suppressed the expression of COX-2 using a preferential COX-2 inhibitor nimesulide and analyzed the sperm from vas deferens for any defects. COX-2 was intensely expressed in the epithelial cells of mice vas deferens and nimesulide was able to effectively suppress most of COX-2 expression. A decrease in PG levels was observed initially but interestingly, the levels tend to rise on sustained suppression of COX-2. The motility of sperm was affected severely after 6h of nimesulide administration that suggested a crucial role of COX-2 towards fertility of mice sperm.

Protective effect of ferulic acid on nicotine-induced DNA damage and cellular changes in cultured rat peripheral blood lymphocytes: a comparison with N-acetylcysteine.

Nicotine is the major pharmacologically active substance in cigarette smoke and plays an important etiological role in the development of lung cancer. Incidence of cancer may be related to oxidative damage to host genome by nicotine. These oxidative actions may be modified by the phytochemicals present in food. The present study describes the protective effect of ferulic acid (FA), a naturally occurring nutritional compound on nicotine-induced DNA damage and cellular changes in cultured rat peripheral blood lymphocytes in comparison with N-acetylcysteine (NAC), a well-known antioxidant. One-hour exposure of lymphocytes to nicotine at the doses of 0.125, 0.25, 0.5, 1, 2, 3 and 4 mM induced a statistically significant dose-dependent increase in the levels of thiobarbituric acid reactive substances (TBARS), a lipid peroxidative marker and decrease in the levels of reduced glutathione (GSH), an important endogenous antioxidant. The lowest concentration eliciting significant damage was 1 mM nicotine and maximum damage was observed with 3 mM concentration. Hence, the test concentration was fixed at 3 mM nicotine. We have used 5 different doses of FA (10, 50, 100, 150 and 300 microM) and NAC (0.25, 0.5, 1, 2 and 4 mM) to test their protective effects. In all the groups, FA and NAC showed a dose-dependent inhibitory effect. Maximum protection was observed at the dose of 150 microM FA and 1mM NAC. So, 150 microM FA and 1mM NAC were used for further studies. There was a significant increase in the levels of lipid peroxidative index (TBARS and hydroperoxides (HP)), severity of DNA damage (evaluated by comet assay) in nicotine-treated group, which were significantly decreased in FA and NAC-treated groups. Nicotine treatment significantly decreased the endogenous antioxidant status viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), GSH, vitamin A, E and C. Co-administration of FA and NAC to nicotine-treated lymphocytes showed a significant increase in the antioxidant status. The protective effect of FA was merely equal to that of NAC effect. FA and NAC treatment alone did not produce any toxicity to the normal lymphocytes at their effective doses. On the whole, there is overwhelming evidence that FA has the ability to modulate DNA damage and a variety of cellular changes that occur during nicotine-induced toxicity in rat peripheral blood lymphocytes.

Ellagic acid, a natural polyphenol protects rat peripheral blood lymphocytes against nicotine-induced cellular and DNA damage in vitro: with the comparison of N-acetylcysteine.

The present work is aimed at evaluating the protective effect of ellagic acid (EA), a natural polyphenolic compound that is widely distributed in fruits and nuts against nicotine-induced toxicity in rat peripheral blood lymphocytes. The effect of EA against nicotine toxicity was compared with N-acetylcysteine (NAC), a well-known antioxidant. Lymphocytes were exposed to nicotine at the doses of 0.125, 0.25, 0.5, 1, 2, 3 and 4 mM for 1h in culture media. Thiobarbituric acid reactive substances (TBARS), a lipid peroxidative marker and reduced glutathione (GSH), as indicative of endogenous antioxidant status were analyzed to fix the optimum dose. The lowest concentration eliciting significant damage was 1 mM nicotine and maximum damage was observed with 3 mM concentration, as evidenced by increased levels of TBARS and decreased levels of GSH. Hence, the test concentration was fixed at 3 mM nicotine. To establish most effective protective support we used five different concentrations of EA (10, 50, 100, 150 and 300 microM) against 3 mM nicotine. A dose-dependent inhibitory effect was observed with all doses of EA. Maximum protection was observed at the dose of 100 microM EA. So, 100 microM dose was used for further studies. We have tested five different concentrations of NAC-0.25, 0.5, 1, 2 and 4 mM to elucidate the optimum protective dose against nicotine toxicity. One millimolar NAC showed a significant protection against nicotine toxicity. Protective effect of EA against nicotine toxicity was elucidated by analyzing the lipid peroxidative index, viz., TBARS, hydroperoxides (HP) and endogenous antioxidant status, viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), Vitamins A, E and C. DNA damage and repair were assessed by using alkaline single-cell microgel electrophoresis (Comet assay) and micronucleus assay. There was a significant increase in the levels of lipid peroxidative index, severity in DNA damage and micronuclei number in nicotine-treated group, which was positively modulated by EA treatment. Antioxidant status was significantly depleted in nicotine-treated group, which was effectively restored by EA treatment. The protection of EA against nicotine toxicity was equally effective to that of NAC. EA and NAC treatment alone did not produce any damage to the normal lymphocytes at their effective doses. These findings suggest the potential use and benefit of EA as a modifier of nicotine-induced genotoxicity.

Comparative effects of curcumin and an analogue of curcumin in carbon tetrachloride-induced hepatotoxicity in rats.

We have evaluated the comparative effect of curcumin (diferuloyl methane) and its analogue [bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione] (BDMC-A) on carbon tetrachloride-induced hepatotoxicity in rats. Administration of carbon tetrachloride (3 ml/kg/week) for three months significantly (P<0.05) increased the levels of marker enzymes such as aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT). The levels of plasma thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides were also significantly (P<0.05) increased. We have observed a significant (P<0.05) decrease in the levels of plasma reduced glutathione (GSH), vitamin C and vitamin E. There was a significant (P<0.05) increase in the levels of TBARS and hydroperoxides in liver and kidney and a significant (P<0.05) decrease in the activities of enzymic antioxidants- superoxide dismutase (SOD), catalase and GSH peroxidase along with GSH in CCl(4)-treated rats. Oral administration of curcumin and BDMC-A to CCl(4)-induced rats for a period of three months significantly (P<0.05) decreased the levels of marker enzymes, plasma TBARS and hydroperoxides and increased the levels of plasma and tissue antioxidants. Histopathological studies of liver also showed protective effect of curcumin and BDMC-A. We have observed thickening of blood vessels and microvesicular fatty changes around the portal triad in CCl(4)-treated rat liver. Treatment with curcumin showed only mild sinusoidal dilatation while with BDMC-A there was only mild portal inflammation. The effect exerted by BDMC-A was found to be more promising than curcumin.

Ferulic Acid modulates altered lipid profiles and prooxidant/antioxidant status in circulation during nicotine-induced toxicity: a dose-dependent study.

Nicotine, an active ingredient of tobacco smoke, is known to induce hyperlipidemia and disturb the prooxidant-antioxidant status. In our study, ferulic acid, a naturally occurring nutritional compound, was tested for its antioxidant and antihyperlipidemic property in a dose-dependent manner against nicotine-induced toxicity in female Wistar rats. We tested three different doses of ferulic acid-10 mg, 20 mg, and 40 mg/kg body weight-for their protective effects. The activities of biochemical marker enzymes lactate dehydrogenase and alkaline phosphatase, levels of peroxidative indices (thiobarbituric acid reactive substances and hydroperoxides), nitric oxide, and circulatory lipids (cholesterol, triglycerides, free fatty acids, and phospholipids) were increased significantly in the nicotine-treated group when compared to normal, which were brought down in ferulic acid-treated groups. The antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, vitamin E, and reduced glutathione) was found to be decreased in the nicotine-treated group, and was significantly increased in ferulic acid-administered groups. Further, ferulic acid also positively modulated the nicotine-induced changes in the micronutrients (zinc and copper) level. The dose 20 mg/kg body weight was found to be more effective than the other two doses. Our data suggest that FA exerts its preventive effects by modulating the degree of lipid peroxidation, antioxidant status, lipid profiles, and trace element levels during nicotine-induced toxicity.

Photoprotective effect of sesamol on UVB-radiation induced oxidative stress in human blood lymphocytes in vitro.

Normal lymphocytes are highly sensitive to the damaging effect of radiation and undergo cell death. In the present study, the photoprotective effect of sesamol, a constituent of sesame oil, has been examined in the UVB-(280-320nm) irradiated human blood lymphocytes. Lymphocytes pretreated with increasing concentrations of sesamol (1, 5 and 10µg/ml) for 30min, were irradiated and lipid peroxidation and antioxidant defense were examined. UVB-irradiated lymphocytes exhibited increased levels of lipid peroxidation and disturbances in antioxidant defense. Sesamol pretreatment resulted in significant reduction in lipid peroxidation marker, thiobarbituric acid reactive substances (TBARS). Further, antioxidants like reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) increased, in a dose-dependent manner, in sesamol pretreated and UVB-irradiated lymphocytes. The maximum dose of sesamol (10µg/ml) normalized the UVB induced lipid peroxidation, indicating the photoprotective effect of sesamol in irradiated lymphocytes.

Restoration of antioxidants by ethanolic Tinospora cordifolia in alloxan-induced diabetic Wistar rats.

The present study investigates the effect of oral administration of an alcoholic extract of Tinospora cordifolia roots on antioxidant defence in alloxan-induced diabetes in rats. A significant increase in the concentration of thiobarbituric acid reactive substances (TBARS) in brain along with a decrease in heart was observed in diabetic rats. Decreased concentration of glutathione (GSH) and decreased activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in heart and brain of diabetic rats were also noted. Alcoholic Tinospora cordifolia root extract (TCREt) administered at a dose of 100 mg/kg to diabetic rats orally for six weeks normalized the antioxidant status of heart and brain. The effect of T. cordifolia root extract was more prominent than glibenclamide (600 microg/kg). Insulin (6 units/kg) restored all the parameters to normal status.

Comparative effects of curcumin and an analog of curcumin on alcohol and PUFA induced oxidative stress.

PURPOSE: Alcoholic liver disease is a major medical complication of alcohol abuse and a common liver disease in western countries. Increasing evidence demonstrates that oxidative stress plays an important etiologic role in the development of alcoholic liver disease. Alcohol alone or in combination with high fat is known to cause oxidative injury. The present study therefore aims at evaluating the protective role of curcumin, an active principle of turmeric and a synthetic analog of curcumin (CA) on alcohol and thermally oxidised sunflower oil (DeltaPUFA) induced oxidative stress. METHODS: Male albino Wistar rats were used for the experimental study. The liver marker enzymes: gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), the lipid peroxidative indices: thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP) and antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) were used as biomarkers for testing the antioxidant potential of the drugs. RESULTS: The liver marker enzymes and lipid peroxidative indices were increased significantly in alcohol, DeltaPUFA and alcohol + DeltaPUFA groups. Administration of curcumin and CA abrograted this effect. The antioxidant status which was decreased in alcohol, DeltaPUFA and alcohol + DeltaPUFA groups was effectively modulated by both curcumin and CA treatment. However, the reduction in oxidative stress was more pronounced in CA treatment groups compared to curcumin. CONCLUSION: In conclusion, these observations show that CA exerts its protective effect by decreasing the lipid peroxidation and improving antioxidant status, thus proving itself as an effective antioxidant.

Curcumin influences hepatic expression patterns of matrix metalloproteinases in liver toxicity.

Hepatic fibrosis is a result of an imbalance between enhanced matrix synthesis and diminished breakdown of connective tissue proteins, the net result of which is increased deposition of Extra Cellular Matrix. In this concept Matrix Metalloproteinases play an important role because their activity is largely responsible for extra cellular matrix breakdown. In the present study we have tested the influence of curcumin, the active principle of turmeric, on matrix metalloproteinase expression during alcohol and thermally oxidised sunflower oil induced liver toxicity. Male albino Wistar rats were used for the study. The matrix metalloproteinase expressions were found to be increased significantly in alcohol as well as thermally oxidised sunflower oil groups and on treatment with curcumin there was a significant decrease. In alcohol + thermally oxidised sunflower oil group, we found a significant decrease in matrix metalloproteinase activities. Administration of curcumin significantly improved their activities. From the results obtained, we could conclude that curcumin influences the hepatic matrix metalloproteinases and effectively protects liver against alcohol and delta PUFA induced toxicity.

Curcumin ameliorates oxidative stress during nicotine-induced lung toxicity in Wistar rats.

Nicotine, a major toxic component of cigarette smoke has been identified as a major risk factor for lung related diseases. In the present study, we evaluated the protective effects of curcumin on lipid peroxidation and antioxidants status in bronchoalveolar lavage fluid (BALF) and bronchoalveolar lavage (BAL) of nicotine treated Wistar rats. Lung toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg body weight (5 days a week, for 22 weeks) and curcumin (80 mg/kg body weight) was given simultaneously by intragastric intubation for 22 weeks. Measurement of biochemical marker enzymes: alkaline phosphatase, lactate dehydrogenase, lipid peroxidation and antioxidants were used to monitor the antiperoxidative effects of curcumin. The increased biochemical marker enzymes as well as lipid peroxides in BALF and BAL of nicotine treated rats was accompanied by a significant decrease in the levels of glutathione, glutathione peroxidase, superoxide dismutase and catalase. Administration of curcumin significantly lowered the biochemical marker enzymes, lipid peroxidation and enhanced the antioxidant status. The results of the present study suggest that curcumin exert its protective effect against nicotine-induced lung toxicity by modulating the biochemical marker enzymes, lipid peroxidation and augmenting antioxidant defense system.

Photo-irradiated curcumin supplementation in streptozotocin-induced diabetic rats: effect on lipid peroxidation.

BACKGROUND: Diabetes mellitus is one of the most common endocrine disorders. A large number of studies are in progress to identify natural substances that are effective in reducing the severity of diabetes. Although a number of drugs are currently marketed, their long-term use can cause a number of adverse effects. MATERIALS AND METHODS: In the present study, we examined the effect of photo-irradiated curcumin on experimental diabetes in order to evaluate the antihyperglycaemic effects of this compound on streptozotocin (40 mg/kg bodyweight)-induced diabetes. Photo-irradiated curcumin was given at a dose of 10, 30 and 80 mg/kg bodyweight. The level of blood glucose was elevated in the diabetic animals. The liver, kidney and brain were assayed for the degree of lipid peroxidation, reduced glutathione content and the activity of enzymic and levels of non-enzymic antioxidants. RESULTS: Antioxidant status decreased in the diabetic animals. Oral administration of photo-irradiated curcumin for 45 days resulted in a significant decrease in the levels of blood glucose, together with near normalisation of enzymic activity and the markers of lipid peroxidation. The best results were obtained in rats treated with 30 mg/kg bodyweight of photo-irradiated curcumin.