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)

Human erythrocytes contain glucosylated and nonglucosylated Cu-Zn-superoxide dismutases which can be separated by boronate affinity chromatography. The percentage of the glucosylated form is significantly increased in the erythrocytes of patients with diabetes as compared to normal erythrocytes. The nonglucosylated form of Cu-Zn-superoxide dismutase, which was washed through the boronate column, was glucosylated in vitro upon exposure to radioactive or non-radioactive D-glucose. Incorporation of D-glucose into the protein was observed, and with the increase in glucosylation, the enzymatic activity decreased, indicating that the glucosylation of the enzyme led to a low active form. This is the first demonstration that superoxide dismutase is glucosylated in erythrocytes and that the glucosylation leads to the inactivation of the enzyme.
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PMID:Increase in the glucosylated form of erythrocyte Cu-Zn-superoxide dismutase in diabetes and close association of the nonenzymatic glucosylation with the enzyme activity. 356 20

Activation of lipid peroxidation was observed in development of alloxan diabetes in young (5-6 months old) and old rats (24-26 months old). Slight inhibition of lipid peroxidation was detected within 10 days of the development of diabetes. The compensatory-adaptation reactions, particularly activation of Zn, Cu-superoxide dismutase, were apparently responsible for the inhibition of lipid peroxidation observed.
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PMID:[Various indices of lipid peroxidation in the blood of alloxan diabetic rats of different ages]. 360 38

It has been established that the pyrogallol autoxidation method for the estimation of the activity of superoxide dismutase (SOD) (EC 1.15.1.1) is superior in precision and sensitivity to a superoxide-generating method (NADH/phenazine methosulfate linked to nitroblue tetrazolium reduction). Reference intervals were established in an urban population in the Far East for SOD activity in erythrocytes using the pyrogallol method, and for glutathione peroxidase (GSH-Px) (EC 1.11.1.9) activity in erythrocytes using a standard glutathione reductase-linked method. On this basis, erythrocyte SOD activities were significantly (P less than 0.05) depressed in cases of visceral cancer, acute myocardial infarct, congestive heart failure, respiratory failure, chronic renal failure, and diabetes mellitus, but within the reference interval in cases of lung cancer and asthma. Erythrocyte GSH-Px activity was significantly (P less than 0.05) depressed in cases of diabetes mellitus and chronic renal failure but elevated in respiratory failure and asthma. GSH-Px and SOD activities were well correlated in patients but not in the reference population.
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PMID:Superoxide dismutase and glutathione peroxidase activities in erythrocytes as indices of oxygen loading in disease: a survey of one hundred cases. 366

Offspring of experimentally induced diabetic animals demonstrate delays in functional, biochemical, and morphological aspects of lung maturation, dealing mainly with the surfactant system. To investigate whether the development of the lung antioxidant enzyme system would be similarly delayed, and thus compromise their tolerance to high O2 exposure, we did the following: 1) produced the diabetic state in rats with streptozotocin injection 24 h after the onset of pregnancy; 2) examined fetal animals from streptozotocin and control rats at gestational days 19, 20, and 21, and newborn animals at day 22 for whole lung disaturated phosphatidylcholine and total phospholipid and for the three antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase; and 3) exposed newborn offspring from streptozotocin-treated and control rats to greater than 95% O2 for several days and their survival, changes in antioxidant enzymes and disaturated phosphatidylcholine and light microscopic findings in response to hyperoxic challenge were compared. Streptozotocin offspring demonstrated essentially no developmental differences in whole lung disaturated phosphatidylcholine, total phospholipid, or antioxidant enzymes activity at the 4 gestational days studied. However, newborns of streptozotocin mothers had consistently superior tolerance to hyperoxic exposure, consisting of increased survival [23/34 (68%) versus 8/26 (31%) in controls, after O2-exposure for 13 days, p less than 0.001], microscopic evidence of reduced inhibition of alveolarization (p less than 0.05), and a trend toward greater antioxidant enzymes response. Thus, in this animal model of experimental diabetes, neither the development of the antioxidant enzymes system nor the development of the surfactant system (as assessed by whole lung disaturated phosphatidylcholine and total phospholipid) appear delayed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lung development in the streptozotocin rat fetus: antioxidant enzymes and survival in high oxygen. 375 56

Enzyme activities of erythrocyte superoxide dismutase (SOD), peroxidase and catalase in groups of diabetic children, the duration of the disease and control qualities were compared with respective values obtained for healthy children. Generally the disease duration was clearly found to affect SOD activity, and catalase activity only a little. No similar influence of either diabetes duration or control was noticed in the case of peroxidase. SOD activity was diminished in diabetics when compared with control subjects, and in turn peroxidase and catalase activities were generally elevated. The diminution in SOD activity may constitute a reason for enhanced pancreatic cells susceptibility to deterioration, followed by the augmentation of peroxidase activity with an 'elaborated' mechanism compensating for the loss of erythrocyte SOD activity.
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PMID:Peroxide metabolism enzymes in diabetic children: relationship to duration and control of diabetes. 378 Mar 10

Alterations in endogenous free radical-scavenging defense mechanisms of rat tissues after body weight loss (induced by starvation for 72 h) associated with hypoinsulinemia were investigated. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and glutathione (GSSG) reductase as well as levels of reduced glutathione (GSH) were examined in several tissues and in erythrocytes. A complex pattern of changes was observed. CAT activities were increased in the heart and pancreas and decreased in the liver. SOD levels were decreased in the heart and increased in the kidney and pancreas. GSH-PX activities were increased only in the kidney, and levels of GSH were decreased only in the liver of starved animals. Erythrocytes from starved animals showed no alterations in the levels of major free radical-scavenging enzymes. However, GSSG reductase levels were lower in erythrocytes from starved animals, and this was associated with an increased susceptibility to H2O2-induced GSH depletion. Paradoxically, H2O2-induced malondialdehyde (MDA) production in erythrocytes from starved animals was lower than that in control erythrocytes. Our results suggest that, in studies of experimental diabetes, attention must be given to the influence of body weight loss per se on the biochemical alterations associated with this disease.
Diabetes 1987 Feb
PMID:Starvation-related alterations in free radical tissue defense mechanisms in rats. 380 31

The contents of Cu, Zn-superoxide dismutase and catalase isolated and purified from the rat liver at the terminal stages of alloxan diabetes were decreased by 40% and 15%, respectively, as compared to the control. It can be concluded that the decrease in superoxide dismutase and catalase activity in experimental alloxan diabetes is mainly connected with the decline in the content of these proteins at the terminal stages of the disease, this, probably, being the result of DNA degradation and RNA transport disturbances under the effect of oxygen active forms.
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PMID:[Quantitative changes in Cu, Zn-superoxide dismutase and catalase isolated from the liver of alloxan diabetic rats]. 382 10

A study was made of levels of malonic dialdehyde, peroxide hemolysis of erythrocytes, superoxide dismutase activity and a tocopherol content for the purpose of investigating the state of lipid peroxidation in 14 patients with type I diabetes mellitus. Correlation between the state of lipid peroxidation and a degree of diabetes mellitus compensation was established. Decompensated diabetes mellitus was characterized by more enhanced lipid peroxidation and tocopherol deficiency.
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PMID:[Lipid peroxidation in patients with type-1 diabetes mellitus]. 395 71

The lipoperoxide values and glutathione peroxidase activity in blood plasma, along with the glutathione peroxidase, catalase and cupro-zinc superoxide dismutase activities in erythrocytes were investigated in 60 women with Type 2 (non-insulin-dependent) diabetes mellitus and in 71 healthy women. The mean lipoperoxide value and the mean plasma glutathione peroxidase activity in the diabetic patients were significantly higher than those in the control subjects (lipoperoxide p less than 0.001, plasma glutathione peroxidase activity p less than 0.01). The plasma glutathione peroxidase activities did not, however, correlate with the plasma lipoperoxide values. The erythrocyte glutathione peroxidase activity was approximately ten times higher than that of the plasma glutathione peroxidase activity, nor did they correlate with each other. In contrast to the findings of other authors on the activities of the protective enzymes in erythrocytes against oxidative damage, there were no significant differences of erythrocytes glutathione peroxidase, catalase and superoxide dismutase activities between diabetic and control women.
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PMID:Increased lipoperoxide value and glutathione peroxidase activity in blood plasma of type 2 (non-insulin-dependent) diabetic women. 404 1

Copper-zinc superoxide dismutase (SOD) is present in relatively high concentrations in the beta-cells of human islets. The activity of the extracted enzyme is partially inhibited upon incubation with the diabetogenic drugs alloxan, streptozotocin, or Vacor. The role of this enzyme in protecting beta-cells against chemically induced diabetes was further investigated. Incubation of intact canine islets with alloxan (0.2 mg/ml) and 4 mM glucose decreased the insulin secretory response by 87% during subsequent exposure to 28 mM glucose. Concomitantly the SOD-specific activity (units of enzyme activity per milligram immunoreactive SOD) decreased 50% in alloxan-exposed islets. When islets were protected from alloxan toxicity by including 28 mM glucose with alloxan, the insulin secretory response and SOD specific activity remained identical to controls. Thus, SOD specific activity correlates with maintenance of beta-cell function. To test the effectiveness of SOD against streptozotocin in vitro, canine islets were incubated 10 min with or without streptozotocin (0.1 mg/ml) with 4 mM glucose; their functional integrity was tested subsequently as the insulin secretory response to 28 mM glucose. Exposure to streptozotocin alone decreased the response by 70%; inclusion of SOD (1.5 mg/ml) before and during exposure to streptozotocin completely prevented this effect. Cyanide-inactivated SOD was not effective. The potential of SOD to prevent streptozotocin-induced diabetes was tested in rats in vivo. SOD injected 10 s or 50 min before streptozotocin prevented or significantly attenuated diabetes. Injection of SOD and streptozotocin simultaneously was much less effective, and cyanide-inactivated SOD was ineffective. No protection was afforded by injection of SOD 12 or 24 h before streptozotocin. Our results support hypotheses that (a) oxygen radicals mediate the beta-cell toxicity of both alloxan and streptozotocin, and (b) beta-cells may be particularly vulnerable to oxygen radical damage.
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PMID:Protective role of superoxide dismutase against diabetogenic drugs. 621 39


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