UMLS:C0011849 - FACTA Search

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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to investigate the effects of treatment with antioxidant stobadine (ST) on the activities of enzymes related with pentose phosphate pathway and glutathione-dependent metabolism and the other markers of oxidative stress in brain and peripheral organs of diabetic rats, and to compare the effects of ST treatment alone with the effects of treatments with another antioxidant vitamin E and ST plus vitamin E. Rats were made diabetic by the injection of streptozotocin (STZ; 55 mg/kg IP), and, 2 days later, some control and diabetic rats were left untreated or treated with ST (24.7 mg/kg/day, orally), vitamin E (400-500 U/kg/day, orally), or both substances together. In the brain, although 6-phosphogluconate dehydrogenase activity (6-PGD) did not change, glucose-6-phosphate dehydrogenase activity (G-6PD) was markedly increased in diabetic rats compared with controls; only combined treatment with ST and vitamin E produced a partial prevention on this alteration. The aorta G-6PD and 6-PGD of diabetic rats were 52% and 36% of control values, respectively. Neither single treatments with each antioxidant nor their combination altered the G-6PD and 6-PGD in aorta of diabetic rats. Glutathione peroxidase (GSHPx) activity was increased by STZ-diabetes in brain, heart, and kidney. In diabetic brain, vitamin E alone or combination with ST kept GSHPx at normal levels. Diabetes-induced stimulation in GSHPx did not decrease in response to the treatment with vitamin E in heart and kidney, but was greatly prevented by ST alone. The activity of glutathione reductase (GR) was decreased in brain and heart of diabetic rats. The treatment with each antioxidant or with a combination of both agents completely prevented this deficiency and resulted in further activation of GR in diabetic tissues. Glutathione S-transferase (GST) activity did not significantly change in diabetic brain and aorta. GST was stimulated by all treatment protocols in the brain of diabetic rats and was depressed in aorta of control rats. Catalase (CAT) was activated in diabetic heart but depressed in diabetic kidney. Diabetes-induced abnormalities in CAT activity did not respond to vitamin E alone in heart, was moderately ameliorated by the treatment with this vitamin in kidney, and was completely prevented by ST alone in both tissues. Superoxide dismutase (SOD) activity of brain and heart was unchanged by the diabetes but inhibited in diabetic kidney after the treatment ST alone or ST plus vitamin E. The lipid peroxidation (MDA) was increased in diabetic brain and heart. ST or vitamin E alone partly prevented diabetes-induced increase in MDA in brain and heart; however, antioxidant combination achieved a completely amelioration in MDA of these tissues of diabetic rats. Kidney MDA levels were similar in control and untreated diabetic animals. ST and vitamin E treatments, when applied separately or together, significantly reduced kidney MDA in both control and diabetic rats; and the combined effect of antioxidants was greater than that of each alone. These results are consistent with the degenerative role of hyperglycemia on cellular reducing equivalent homeostasis and antioxidant defense, and provide further evidence that pharmacological intervention of different antioxidants may have significant implications in the prevention of the prooxidant feature of diabetes and protects redox status of the cells.
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PMID:Pentose phosphate pathway, glutathione-dependent enzymes and antioxidant defense during oxidative stress in diabetic rodent brain and peripheral organs: effects of stobadine and vitamin E. 1271 33

The effect of sulfur dioxide (SO2) on brain antioxidant status, lipid peroxidation, and somatosensory evoked potentials (SEPs) was investigated in diabetic rats. A total of 40 rats were divided into 4 equal groups: control (C), SO2 + C (SO2), diabetic (D), and SO2 + D (DSO2). Experimental diabetes mellitus was induced by i.v. injection of alloxan at a dose of 50 mg/kg body weight. Ten ppm SO2 was administered to the rats in the sulfur dioxide groups (SO2 and DSO2) in an exposure chamber. Exposure occurred 1 hr/day, 7 days/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. Although SO2 exposure markedly increased copper, zinc Superoxide dismutase activity, it significantly decreased glutathione peroxidase activity in both the diabetic and nondiabetic groups, compared with the C group. Brain catalase activity was unaltered; however, brain thiobarbituric acid reactive substances (TBARS) were elevated in all experimental groups with respect to the C group. SEP components P1, N1, P2, and N2 were significantly increased in all experimental groups, compared with the C group, and these components were also prolonged in the DSO2 group with respect to the other groups. The authors' findings suggest that exposure to SO2, because it increases lipid peroxidation, can change antioxidant enzyme activities and affect SEP components in diabetic rats.
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PMID:Changes in somatosensory evoked potentials, lipid peroxidation, and antioxidant enzymes in experimental diabetes: effect of sulfur dioxide. 1274 14

Increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the pathogenesis and progression of diabetes mellitus and other oxidant-related diseases. This study was designed to determine whether alpha-lipoic acid, which has been shown to have substantial antioxidant properties, when administered (10 mg/kg ip) once daily for 14 days to normal and diabetic female Sprague-Dawley rats would prevent diabetes-induced changes in biomarkers of oxidative stress in liver, kidney and heart. Serum glucose concentrations, aspartate aminotransferase activity, and glycated hemoglobin levels, which were increased in diabetes, were not significantly altered by alpha-lipoic acid treatment. Normal rats treated with a high dose of alpha-lipoic acid (50 mg/kg) survived but diabetic rats on similar treatment died during the course of the experiment. The activity of glutathione peroxidase was increased in livers of normal rats treated with alpha-lipoic acid, but decreased in diabetic rats after alpha-lipoic acid treatment. Hepatic catalase activity was decreased in both normal and diabetic rats after alpha-lipoic acid treatment. Concentrations of reduced glutathione and glutathione disulfide in liver were increased after alpha-lipoic acid treatment of normal rats, but were not altered in diabetics. In kidney, glutathione peroxidase activity was elevated in diabetic rats, and in both normal and diabetic animals after alpha-lipoic acid treatment. Superoxide dismutase activity in heart was decreased in diabetic rats but normalized after treatment with alpha-lipoic acid; other cardiac enzyme activities were not influenced by either diabetes or antioxidant treatment. These results suggest that after 14 days of treatment with an appropriate pharmacological dose, alpha-lipoic acid may reduce oxidative stress in STZ-induced diabetic rats, perhaps by modulating the thiol status of the cells.
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PMID:Effects of alpha-lipoic acid on biomarkers of oxidative stress in streptozotocin-induced diabetic rats. 1283 33

Plasma vitamin A, C and E levels and erythrocyte antioxidant enzyme activities were investigated in type I and type II diabetic subjects with and without complications, i.e., hypertension, coronary artery disease and renal failure. Reverse phase HPLC was used to quantify vitamin A and E levels. We observed that the vitamin C levels were not significantly different between control and diabetic subjects. However, vitamin A and E levels were significantly lower in type I and type II diabetic subjects compared to controls. Superoxide dismutase (SOD) activity was significantly lower in type II, but not in type I, diabetic patients compared to controls. Interestingly, glutathione reductase and peroxidase activities were diminished in type I, but not in type II, diabetic subjects as compared to controls. Catalase activity was lower in both types of diabetic patients in comparison with their respective controls. Altogether these results suggest that diabetes mellitus may be associated with altered antioxidant status regardless to various complications.
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PMID:Antioxidant status and levels of different vitamins determined by high performance liquid chromatography in diabetic subjects with multiple complications. 1287 Jun 98

Concentration of lipid peroxidation products and antioxidant enzyme activities in rat brain and erythrocytes and the effects of nicotinamide and nicotinoyl-GABA administration on these parameters were estimated on 21st day of streptozotocin-induced diabetes. It was demonstrated more then two-fold diabetes-induced accumulation of conjugated dienes and malondialdehyde in tissues studied. Superoxide dismutase and glutathione reductase activities of both brain homogenate and erythrocytes as well as catalase and glutathione peroxidase activities of brain homogenate were shown to decrease significantly in diabetic rats, meanwhile, catalase activity of erythrocytes was increased and glutathione peroxidase unchanged. So the correlation between changes in enzymatic antioxidant system in brain and erythocytes failed to be found. Alterations observed were virtually prevented by the course of nicotinamide and nicotinoyl-GABA treatment. The results suggested that the suppression of antioxidant system could be primary biochemical disturbance in diabetic neuropathy progression. It was shown that the antioxidant efficacy of nicotinoyl-GABA is lower than that of nicotinamide. It was suggested that the mechanism of antioxidant action of nicotinamide and its structural analogue consists of both scavenging of lipid peroxides and NAD biosynthesis that leads to activation and normalization of altered energy and lipid metabolism.
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PMID:[Oxidative stress correction by nicotinamide and nicotynol-GABA in diabetic neuropathy]. 1291 62

(1) The aim of the present study was to investigate the causal relationship between peroxisome proliferator-activated receptor (PPAR) and endothelium-dependent relaxation in streptozotocin (STZ)-induced diabetic rats. (2) Acetylcholine (ACh)-induced endothelium-dependent relaxation was significantly weaker in diabetic rats than in age-matched controls. The decreased relaxation in diabetes was improved by the chronic administration of bezafibrate (30 mg kg-1, p.o., 4 weeks). (3) The expressions of the mRNAs for PPARalpha and PPARgamma were significantly decreased in STZ-induced diabetic rats (compared with the controls) and this decrease was restored partially, but not completely, by the chronic administration of bezafibrate. (4) Superoxide dismutase activity in the aorta was not significantly different between diabetic rats and bezafibrate-treated diabetic rats. (5) The expression of the mRNA for the p22phox subunit of NAD(P)H oxidase was significantly higher in diabetics than in controls, but it was lower in bezafibrate-treated diabetic rats than in nontreated diabetic rats. Although the expression of the mRNA for prepro ET-1 (ppET-1) was markedly increased in diabetic rats (compared with controls), this increase was prevented to a significant extent by the chronic administration of bezafibrate. (6) These results suggest that downregulations of PPARalpha and PPARgamma may lead to an increased expression of ppET-1 mRNA in diabetic states and this increment may trigger endothelial dysfunction.
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PMID:Relationship between peroxisome proliferator-activated receptors (PPAR alpha and PPAR gamma) and endothelium-dependent relaxation in streptozotocin-induced diabetic rats. 1296 31

Aminoacetone (AA) is a threonine and glycine metabolite overproduced and recently implicated as a contributing source of methylglyoxal (MG) in conditions of ketosis. Oxidation of AA to MG, NH4+, and H2O2 has been reported to be catalyzed by a copper-dependent semicarbazide sensitive amine oxidase (SSAO) as well as by copper- and iron ion-catalyzed reactions with oxygen. We previously demonstrated that AA-generated O2*-. and enoyl radical (AA*) induce dose-dependent Fe(II) release from horse spleen ferritin (HoSF); no reaction occurs under nitrogen. In the present study we further explored the mechanism of iron release and the effect of AA on the ferritin apoprotein. Iron chelators such as EDTA, ATP and citrate, and phosphate accelerated AA-promoted iron release from HoSF, which was faster in horse spleen isoferritins containing larger amounts of phosphate in the core. Incubation of apoferritin with AA (2.5-50 mM, after 6 h) changes the apoprotein electrophoretic behavior, suggesting a structural modification of the apoprotein by AA-generated ROS. Superoxide dismutase (SOD) was able to partially protect apoferritin from structural modification whereas catalase, ethanol, and mannitol were ineffective in protection. Incubation of apoferritin with AA (1-10 mM) produced a dose-dependent decrease in tryptophan fluorescence (13-30%, after 5 h), and a partial depletion of protein thiols (29% after 24 h). The AA promoted damage to apoferritin produced a 40% decrease in apoprotein ferroxidase activity and an 80% decrease in its iron uptake ability. The current findings of changes in ferritin and apoferritin may contribute to intracellular iron-induced oxidative stress during AA formation in ketosis and diabetes mellitus.
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PMID:Aminoacetone induces loss of ferritin ferroxidase and iron uptake activities. 1470 1

Diabetes is associated with impaired endothelium-dependent relaxation. We questioned whether administration of superoxide dismutase (superoxide: superoxide oxidoreductase, EC 1.15.1.1) entrapped in long-circulating liposomes improves the vascular reactivity of the resistance arteries. Using the myograph technique, the vasodilation in response to acetylcholine was measured in mesenteric resistance arteries isolated from diabetic or normal hamsters treated for 3 days with superoxide dismutase entrapped in liposomes, with the same concentrations of free superoxide dismutase and plain liposomes, or untreated. Superoxide dismutase activity and nitric oxide (NO) levels were assayed by spectrophotometry, superoxide dismutase levels by Western blot and the role of N(pi)-nitro-L-arginine ethylester (L-NAME) on vasodilation by the myograph technique. Our data revealed that: (i) superoxide dismutase entrapped in liposomes restored to a great extent the endothelium-dependent relaxation of diabetic hamster resistance arteries; (ii) in superoxide dismutase entrapped in liposomes-treated diabetic animals, the activity and the level of superoxide dismutase in arterial homogenates as well as the serum nitrite levels were significantly higher than those in untreated hamsters or hamsters treated with free superoxide dismutase and plain liposomes: (iii) L-NAME inhibited the response of arteries to acetylcholine in superoxide dismutase entrapped in liposomes-treated diabetic hamsters. These results suggest that superoxide dismutase entrapped in liposomes is effective in scavenging superoxide anions, increases nitric oxide bioactivity and improves the vasorelaxation of resistance arteries in diabetic hamsters.
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PMID:Superoxide dismutase entrapped-liposomes restore the impaired endothelium-dependent relaxation of resistance arteries in experimental diabetes. 1472 88

Oxidative stress induced by alloxan has been shown to damage pancreatic beta-cell and produce hyperglycemia in rats. Aegle marmelos leaf extract is being used in Ayurveda as a medicine for diabetes. The present study examined the action of Aegle marmelos against experimental diabetes as well as the antioxidant potential of the drug. A methanolic extract of Aegle marmelos was found to reduce blood sugar in alloxan diabetic rats. Reduction in blood sugar could be seen from 6th day after continuous administration of the extract and on 12th day sugar levels were found to be reduced by 54%. Oxidative stress produced by alloxan was found to be significantly lowered by the administration of Aegle marmelos extract. This was evident from a significant decrease in lipid peroxidation, conjugated diene and hydroperoxide levels in serum as well as in liver induced by alloxan. Catalase and glutathione peroxidase activity in blood and liver were found to be increased from 9th day onwards after drug administration. Superoxide dismutase and glutathione levels were found to be increased only on 12th day. These results indicate that Aegle marmelos extract effectively reduced the oxidative stress induced by alloxan and produced a reduction in blood sugar.
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PMID:Antidiabetic activity of Aegle marmelos and its relationship with its antioxidant properties. 1527 Mar 73

In the present study changes in oxidative stress and vascular reactivity in aortic rings of chronic streptozotocin-diabetic (STZ-CON) and nondiabetic (ND-CON) rats is studied at 4 weekly intervals up to 24 weeks. The effect of chronic curcumin (200 mg/kg) treatment was also studied. Blood glucose and blood pressure levels were significantly higher in the STZ-CON group and curcumin administration had no significant effect on it. Superoxide dismutase and catalase activity were either unchanged or significantly increased during the early stage of diabetes whereas during the medium and late stage were significantly reduced. Reduced glutathione and lipid peroxidation levels significantly decreased as time after STZ administration increased. Phenylephrine (PE)-induced contraction was significantly (P < 0.05) increased during the early stage of diabetes, whereas it was significantly (P < 0.05) reduced at the medium and late stage of diabetes. Acetylcholine (Ach)-induced relaxation significantly decreased with respect to time after STZ administration. Sodium nitroprusside (SNP)-induced relaxation was unaltered up to initial stage but after medium stage there was a rightward shift and the pD2 value significantly decreased. Though curcumin treatment had no significant effect on superoxide dismutase, catalase, and reduced glutathione levels, it significantly reduced lipid peroxidation compared with diabetic control. Curcumin treatment attenuated the phenylephrine-induced increase in contraction during the early stage. However, curcumin treatment had no significant effect at the medium and late stage. Though curcumin administration improved Ach-induced relaxation it did not restore it to normal. Inability of curcumin to prevent oxidative stress during the late stage may be due to the fact that chronic diabetes (hyperglycemia) leads to excessive production of free radicals. Hence the present study shows that variations reported in antioxidant enzymes and vascular reactivity are due to the duration of diabetes or time after diabetes induction in STZ model and this can not be completely reversed by chronic treatment with curcumin.
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PMID:Time-dependent changes in antioxidant enzymes and vascular reactivity of aorta in streptozotocin-induced diabetic rats treated with curcumin. 1622 78

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