Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of lipid peroxidation in liver, kidney, brain and blood, liver glutathione (GSH) and several enzymes in liver tissue associated with antioxidant defence mechanism, namely Catalase (EC: 1.11.1.6), GSH reductase (EC:1.6.4.2) and GSH-S-transferase (EC: 2.5.1.18), were investigated in streptozotocin-induced diabetic rats. The single intraperitoneal injection of streptozotocin (65 mg/kg) caused a four-, eight- and seven-fold increase in lipid peroxidation in brain, liver and kidney, respectively. A decline in GSH levels both in blood (two-fold) and liver (16%) compared with normal counterparts was also observed. A marginal increase in catalase activity, a 20% decrease in GSH reductase and an increase of GSH-S-transferase activity was also found in this experimental diabetic condition. These results suggest experimental diabetes, induced by streptozotocin, can produce biochemical changes not only in pancreas but also in liver, kidney and brain tissue.
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PMID:Lipid peroxidation, glutathione levels and changes in glutathione-related enzyme activities in streptozotocin-induced diabetic rats. 820 Jun 86

Aminoguanidine (AG) has been proposed as a drug of potential benefit in prophylaxis of the complications of diabetes. We show here that AG irreversibly inhibits catalase with an efficacy similar to aminotriazole. AG also produces hydrogen peroxide, in a transition metal-catalysed process which may be partially dependent upon prior hydrolysis of AG to semicarbazide and hydrazine. These observations may be of importance in proposals for the long term administration of AG in diabetes.
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PMID:Aminoguanidine: a drug proposed for prophylaxis in diabetes inhibits catalase and generates hydrogen peroxide in vitro. 821 63

The effects of diabetes on levels of lipid peroxides and glycolipids in brain were studied in alloxan (18 mg/100 g body weight) diabetic rats. Free fatty acid (FFA) and malondialdehyde (MDA) levels were increased in the brains of diabetic animals. On the other hand, activities of the antioxidative enzymes catalase and superoxide dismutase (SOD) were decreased. The study also showed elevated levels of most of the glycolipid fractions except gangliosides, which were found to decrease in diabetic brain. Administration of insulin to diabetic animals results in the restoration of these parameters to normal levels. These changes observed in diabetic brain may be responsible for the increased frequency of stroke in diabetes.
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PMID:Effect of diabetes on levels of lipid peroxides and glycolipids in rat brain. 823 39

The influence of acute diabetes (8 days), induced by streptozotocin (45 mg.kg-1 body weight) on myocardial and renal antioxidative conditions was investigated. The animals were given subtherapeutical doses of insulin (Interdep 6 U. kg-1 body weight, s.c.). Considerably increased levels of malondialdehyde (MDA), as well as of superoxide dismutase (SOD) and catalase (CAT) activity were found in the myocardium of diabetic animals. The oxidized glutathione (GSSG) level and glutathione peroxidase (GSH-PX) activity remained unchanged. The reduced glutathione (GSH) level as well as the activity of glutathione S-transferase (GST) were significantly lower. The activity of GSH-PX in the kidneys of diabetic rats increased by 60% and that of GST by 105%, respectively. CAT and SOD activity values were unchanged.
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PMID:Antioxidative state of the myocardium and kidneys in acute diabetic rats. 828 Jul 23

The study included 16 patients with diabetes mellitus (DM) type 1 and 15 healthy controls. By the moment of examination the patients had achieved subcompensation. 10 patients developed diabetic vascular complications. The patients received biosynthetic insulins Humulin S, Humulin I, Humulin M3. Pretreatment glycemia in the patients surpassed that in the controls, MDA red cell levels per ml of hemolysate were higher by 121% and 130% per protein 1 mg. MDA measured equal both in angiopathy patients and those without it. The activity of the antioxidant enzymes in DM patients was similar to control indices. Human insulin administration reduced red cell MDA levels both in angiopathy and free of it patients, though in the former MDA remained higher than normal, while in the latter normal levels are obtained. The parameters of the antioxidant defense enzymes changed on the treatment week 12: catalase activity rose by 41%, that of superoxide dismutase and glutathione peroxidase lowered by 35 and 65%, respectively. Variations in these enzymes activity showed no dependence on vascular complications.
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PMID:[Lipid peroxidation and the antioxidant protection of the erythrocytes in diabetes mellitus patients]. 829 27

Arteriolar dilation to endothelium-derived relaxing factor (EDRF) is suppressed early in diabetes mellitus. The purpose of this study was to determine whether acute exposure to a hyperglycemic media can suppress EDRF function of normal arterioles. Dilation of intestinal arterioles to iontophoretically applied acetylcholine (ACh) and nitroprusside was measured in normoglycemic rats before and after 1 h of topical exposure to isotonic solutions containing D-glucose concentrations of 200, 300, and 500 mg/100 ml. Exposure to a D-glucose concentration of 200 mg/100 ml had no effect on vasodilation to ACh. D-Glucose concentrations of both 300 and 500 mg/100 ml caused significant suppression of the responses: for example, at the approximate 50% effective dosage (100 nA), the dilatory response was decreased by 60% at a D-glucose concentration of 300 mg/100 ml and 55% at a D-glucose concentration of 500 mg/100 ml. Responses to nitroprusside were not significantly (P < 0.05) impaired after exposure to D-glucose concentrations of 200, 300, or 500 mg/100 ml. Exposure to an isotonic L-glucose concentration of 500 mg/100 ml for 1 h had no significant (P > 0.05) effect on responses to ACh. Pretreatment with superoxide dismutase, catalase, indomethacin, or meclofenamic acid preserved EDRF-mediated vasodilation during exposure to a D-glucose concentration of 500 mg/100 ml at almost all the ACh dosages tested. These results indicate that oxygen radicals formed in part by increased eicosanoid synthesis during exposure to D-glucose hyperglycemia interfere with the EDRF mechanism before its action on the microvascular smooth muscle.
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PMID:Topical hyperglycemia rapidly suppresses EDRF-mediated vasodilation of normal rat arterioles. 834 36

Lithium is widely used for treatment of behavioral disorders and has been shown to possess insulin-mimetic properties. The present study examines the in vivo effects of lithium alone, as well as in combination with vanadate (a potent insulin-mimetic agent), on the altered antioxidant status in the liver and kidney of diabetic rats. The elevated blood glucose levels in diabetic rats were about 50% restored by oral administration of lithium (0.3 mg/ml) and were completely normalized following vanadate addition (0.05 mg/ml) to lithium. Lithium therapy effectively normalized the decreased activities of catalase (CAT) and glutathione peroxidase (GSH-PX) but could not restore the lowered superoxide dismutase (SOD) in the liver of diabetic rats; while in kidney, the treatment proved to be ineffective. Inclusion of vanadate produced synergistic effect and caused partial restoration of the altered CAT, GSH-PX and CuZn-SOD levels in diabetic kidney and the depressed SOD activity in diabetic liver. These results suggest that lithium therapy may prove effective in improving the impaired antioxidant status during diabetes and vanadate supplementation at a low dose potentiates the effectiveness of lithium action.
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PMID:Insulin like effects of lithium and vanadate on the altered antioxidant status of diabetic rats. 835 10

In vivo effects of vanadate on the antioxidant status of control and alloxan diabetic rats liver were examined. The increased oxidative stress during diabetes caused a decline in the activities of glutathione peroxidase (GPx), catalase (CAT), CuZn superoxide dismutase (CuZn-SOD) and Mn-superoxide dismutase (Mn-SOD) in the liver. Reduced glutathione (GSH) was also depleted, but the level of oxidized glutathione and glutathione reductase activity remained unchanged in the livers of diabetic rats. Vanadate treatment of diabetic rats (0.6 mg/mL in drinking water) resulted in almost complete restoration of GPx and Mn-SOD but caused only a partial restoration of CuZn-SOD. However, CAT and GSH were found to be lowered further in vanadate-treated diabetic rats as compared to untreated diabetic rat. Similar decreases in CAT and GSH levels were also observed in the vanadate-treated controls. These results suggest that vanadate, an insulin-mimetic agent, effectively normalized hyperglycemia, but unlike insulin, could not completely restore the altered endogenous defence mechanisms in diabetic liver.
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PMID:Impaired antioxidant status in diabetic rat liver. Effect of vanadate. 844 52

Insulin-dependent diabetes (IDD) in the nonobese diabetic (NOD) mouse is believed to result from the specific autoimmune destruction of pancreatic beta cells. The frequency of diabetes in the NOD mouse is sex-dependent, with approximately 90% of females and 40% of males developing clinical diabetes by 40 weeks of age. Recently, attention has focused on determining possible mechanisms for beta cell destruction. One potential mechanism is the toxic effect of free oxygen radicals produced as a result of the influx of inflammatory cells into the pancreas. A deficiency in available antioxidant enzymes could form a basis for diabetes susceptibility. To test the feasibility of this idea, we have compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in isolated islets, pancreas, and other tissues of age- and sex-matched NOD, BALB/c, C57BL/10, and B10.GD mice. Enzyme profiles revealed that female NOD mice do not differ significantly in antioxidant enzyme activity from females of the other inbred strains. However, antioxidant enzyme activity in females was generally lower than in males regardless of mouse strain. While isolated islet cells exhibited somewhat lower levels of enzyme activity than other tissues, the islets of NOD mice proved to be no more deficient than those of BALB/c mice. Therefore, it is unlikely that any toxic effect of free oxygen radicals on the beta cells of NOD mice results directly or solely from an antioxidant enzyme deficiency. Nevertheless, one possible explanation for the lower incidence of diabetes in NOD males versus females may be the inherently higher male antioxidant enzyme activities.
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PMID:Antioxidant enzyme activities in IDD-prone and IDD-resistant mice: a comparative study. 846 25

We hypothesized that oxygen free radicals (OFRs) may be involved in pathogenesis of diabetic complications. We therefore investigated the levels of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) and activity of antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT)] in tissues and blood of streptozotocin (STZ)-induced diabetic rats. The animals were divided into two groups: control and diabetic. After 10 weeks (wks) of diabetes the animals were sacrificed and liver, heart, pancreas, kidney and blood were collected for measurement of various biochemical parameters. Diabetes was associated with a significant increase in TBARS in pancreas, heart and blood. The activity of CAT increased in liver, heart and blood but decreased in kidney. GSH-Px activity increased in pancreas and kidney while SOD activity increased in liver, heart and pancreas. Our findings suggest that oxidative stress occurs in diabetic state and that oxidative damage to tissues may be a contributory factor in complications associated with diabetes.
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PMID:Lipid peroxidation and activity of antioxidant enzymes in diabetic rats. 856 56


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