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

Glucose may oxidise under physiological conditions and lead to the production of protein reactive ketoaldehydes, hydrogen peroxide and highly reactive oxidants. Glucose is thus able to modify proteins by the attachment of its oxidation derived aldehydes, leading to the development of novel protein fluorophores, as well as fragment protein via free radical mechanisms. The fragmentation of protein by glucose is inhibitable by metal chelators such as diethylenetriamine pentaacetic acid (DETAPAC) and free radical scavengers such as benzoic acid, and sorbitol. The enzymic antioxidant, catalase, also inhibits protein fragmentation. Protein glycation and protein oxidation are inextricably linked. Indeed, using boronate affinity chromatography to separate glycated from non-glycated material, we demonstrate that proteins which are glycated exhibit an enhanced tryptophan oxidation. Our observation that both glycation and oxidation occur simultaneously further supports the hypothesis that tissue damage associated with diabetes and ageing has an oxidative origin.
 ...
PMID:Oxidative glycation and free radical production: a causal mechanism of diabetic complications. 164 79

Blood antioxidant system parameters were examined in elderly subjects. The authors have developed methods for measurements of catalase, superoxide dismutase, and lipid peroxidation products. They introduce a new factor 'F' that is supposed to characterize the blood antioxidant system; this factor is based on the values of catalase and superoxide dismutase activities and the intensity of lipid peroxidation. The authors come to a conclusion that the blood antioxidant and oxidant systems may be more accurately described with the use of this new factor F. In case of an abdominal tumor whole blood catalase level is elevated and superoxide dismutase activity significantly reduced. Factor F values were found extremely low before death, therefore this factor may be considered an important criterion of a critical state. The blood antioxidant parameters of patients with diabetes mellitus and essential hypertension did not much differ from those of age-matched healthy subjects.
 ...
PMID:[Determination of the antioxidant properties of the blood and their diagnostic significance in the elderly]. 172 48

Free radicals have recently been proposed to play a role in the development of diabetic retinopathy. Ischaemia and hyperglycaemia followed by recirculation have been suggested to initiate free radical production in other tissues and the aim of the present study was to examine whether this could also be the case in the retina. The present study showed retinal cell damage, as measured by pycnotic cells, to be more pronounced when ischaemia was combined with hyperglycaemia than when combined with normoglycaemia. As an indication of free radical production, catalase activity was measured, reflecting the production of hydrogen peroxide (H2O2). Small amounts of H2O2 were found to be generated in the normal retina, but did not increase during ischaemia and hyperglycaemia followed by recirculation. It thus seems, as if hyperglycaemia aggravates the harmful effects of ischaemia, but with the methods used, there does not seem to be any increase in free radical production (as measured by H2O2 production) in normal rat retina during ischaemic and hyperglycaemic conditions.
Diabetes Res 1991 Jan
PMID:Hydrogen peroxide production in ischaemic retina: influence of hyperglycaemia and postischaemic oxygen tension. 181 95

Incubation of corneal collagen type I with glucose in the presence of transition metal ions (copper, iron) results in the formation of collagen aggregates insoluble in 6 M urea, and in 2% sodium dodecyl sulfate + 5% beta-mercaptoethanol. The reaction is mediated by hydrogen peroxide and transition metals since it is inhibited by catalase and by the chelating agent diethylenetriaminepentaacetic acid. Comparative studies showed that copper is more efficient than iron and that the reaction proceeds more rapidly with ribose than with glucose. The data support a mechanism involving transition metal ion catalyzed autoxidation of glucose (and possibly of Amadori products) with generation of superoxide radical. Superoxide dismutation produces hydrogen peroxide, which then generates hydroxyl radicals in the presence of transition metal ions (Fenton reaction). Hydroxyl radical attack is known to lead to cross-linking, which is enhanced in glycated proteins. The experimental data presented are consistent with in vivo alteration of collagen properties during normal aging and with the acceleration of similar changes in diabetes mellitus.
 ...
PMID:The role of nonenzymatic glycosylation, transition metals, and free radicals in the formation of collagen aggregates. 189 43

The activities of enzymes involved in cellular defence mechanisms such as superoxide dismutase, catalase, glutathione peroxidase and glutathione level have been found to be altered in experimental diabetes. Rats were made diabetic by a single i.v. injection of streptozotocin (55 mg/kg body weight) in citrate buffer. After the onset of diabetes, the diabetic rats were treated with sodium orthovanadate (0.3 mg/ml) for 15 days. Decreased activities of glutathione peroxidase, catalase, superoxide dismutase and glutathione content found in diabetic rats were corrected to near normal. The altered levels of plasma lipid peroxide, glycoproteins and erythrocyte membrane phospholipids in diabetic rats were restored to control levels by vanadate treatment. These observations clearly indicate the antioxidant potential of vanadate on experimental diabetes.
 ...
PMID:Antioxidant effect of vanadate on experimental diabetic rats. 208 29

Isovolumically perfused control and chronic diabetic rat hearts were subjected to 20 min of global ischemia plus 30 min of reperfusion at preischemic flow rates. Recoveries of contractile function during reperfusion were similar in both groups. Addition of arachidonic acid produced profound postischemic dysfunction in nondiabetic hearts (isovolumic minute work = 19 +/- 8 vs. 86 +/- 10% of preischemic levels after 30 min), whereas arachidonic acid had no detrimental effect in diabetic hearts. Arachidonic acid also augmented endogenous prostacyclin release in control hearts (untreated 2.28 +/- 0.23 ng/ml; arachidonic acid 4.07 +/- 0.22 ng/ml) but failed to alter postischemic prostacyclin release in diabetic hearts. The arachidonic acid-induced postischemic dysfunction was significantly attenuated by coadministration of the oxygen free radical scavengers, superoxide dismutase plus catalase, but not by indomethacin. Thus arachidonic acid-induced dysfunction in normal hearts appears to be related, in part, to free radical production. The intrinsic capacity of the heart to synthesize prostacyclin as a result of ischemia and reperfusion does not appear to be impaired by diabetes. In contrast, the arachidonic acid-induced increase in prostacyclin following ischemia is blunted in the diabetic heart. Although chronic diabetic hearts showed increased tolerance to arachidonic acid-induced dysfunction during reperfusion, a defect in prostacyclin stimulation may place the diabetic at greater risk of complications of ischemic reperfusion in vivo by reducing the capacity to adequately respond to the aggregatory and vasospastic actions of increased circulating thromboxane consequent to myocardial ischemia and reperfusion.
 ...
PMID:Arachidonic acid causes postischemic dysfunction in control but not diabetic hearts. 210 41

An intravenous glucose sensor was implanted in six dogs for 1-15 wk. The glucose sensor is a flexible cylinder, approximately 0.2 cm diam and 30 cm long, with a tip containing immobilized glucose oxidase and catalase coupled to a potentiostatic O2 sensor. The sensor and a similar O2 reference sensor were implanted in the superior vena cava near the entrance of the right atrium. The sensor response was conveyed externally either by a telemetry system implanted nearby, surgically accessed leads, or chronically maintained percutaneous leads. Summing over the six implants, there was a total implantation period of 333 days during which glucose sensors were functional on demand. The sensor response showed agreement with conventionally assayed blood samples after accounting for a response lag. Sensor response to glucose showed little change over the implant period. Biocompatibility, enzyme lifetime, O2 availability, O2 sensor stability, and biochemical interference were not limitations. Results demonstrated that this sensor can function effectively as an implant in dogs for a period of months and has the potential for long-term operation.
Diabetes 1990 Dec
PMID:Application of chronic intravascular blood glucose sensor in dogs. 224 76

Alterations in superoxide dismutase activity, observed in erythrocytes of children with insulin-dependent form of diabetes mellitus, depended on the age of patients, severity and degree of the disease compensation. Content of lipid peroxidation products was also dissimilar in compensated and decompensated forms of diabetes mellitus. Activity of catalase in erythrocytes of patients was similar to corresponding values of healthy children and did not depend on the disease stage and severity. Estimation of superoxide dismutase activity and content of diene ketons were most suitable patterns for monitoring treatment of diabetes in children.
 ...
PMID:[Activity of antioxidative enzymes and lipid peroxidation in erythrocytes of children with diabetes mellitus]. 234 73

Eicosanoid metabolism is altered by diabetes. However, postischemic responses of diabetic hearts (DH) to eicosanoids such as prostacyclin are unknown. a prostacyclin analogue iloprost (Ilo) was given to isovolumically beating rat hearts during 20 min of total global ischemia and 30 min of reperfusion. Acute DH (48 h) but not chronic DH (2 mo) had pronounced postischemic dysfunction (developed pressure = 22 +/- 11%), which was completely reversed by 3 X 10(-8) M Ilo (developed pressure = 113 +/- 15%). Ilo also stimulated endogenous prostacyclin release in postischemic control hearts (CH) but not acute or chronic DH. Ilo significantly decreased postischemic recovery in CH (from 67 +/- 11 to 15 +/- 4%), which was partially blocked by the coadministration of the calcium-entry blocker diltiazem or almost completely reversed by the free radical scavengers superoxide dismutase plus catalase (100 U/ml). These data suggest that Ilo may promote functional recovery in DH at concentrations that produce dysfunction in CH. Furthermore, Ilo may induce dysfunction in CH by a calcium ionophoretic action, which appears depressed in diabetes, and by concomitant free radical production (presumably via prostaglandin hydroperoxidases) during Ilo-stimulated endogenous prostacyclin synthesis.
 ...
PMID:Diabetes alters postischemic response to a prostacyclin mimetic. 247 Feb 63

Spontaneous diabetes in the non-obese diabetic (NOD) mice is a CD4 T cell-dependent process. We have suggested that specific beta cell destruction results from free radical production at the site of islet inflammation; oxygen radicals are produced by activated inflammatory cells. We reported here that in vivo treatment of spontaneously diabetic NOD mice with the enzyme superoxide dismutase (2000 U for seven injections) and catalase (40,000 U for seven injections) protects islet tissue from disease recurrence following transplantation into spontaneously diabetic mice. Similar results were obtained when animals were treated with either enzyme alone. This effect was dose-dependent and little protection was observed when the dose of enzyme was reduced four-fold. These results indicate that oxygen metabolites, specially superoxide and hydrogen peroxide, are directly involved in the pathogenesis of immunology mediated diabetes.
 ...
PMID:Involvement of O2 radicals in 'autoimmune' diabetes. 254 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>