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

Superoxide dismutase, glutathione peroxidase and glutathione reductase activities were measured in erythrocytes of 214 young patients with insulin-dependent diabetes and 37 healthy subjects with similar age and sex distribution. The diabetic patients were divided into groups and subgroups according to sex, age, duration of disease, existence of diabetes complications and family history of atherogenic risks. Data analysis was performed by comparing enzyme activities in subgroups according to the degree of diabetes control and the plasmatic level of various lipid fractions. Results showed that superoxide dismutase, glutathione peroxidase and glutathione reductase activities in young diabetic patients were similar to those in controls, except for patients with retinopathy, whose glutathione peroxidase activity was decreased. This last finding might suggest that there is a relationship between the development of diabetic microvascular complications and the accumulation of free radicals and peroxide lipids.
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PMID:[Antioxidant enzymes in insulin-dependent diabetes in the child and adolescent]. 208 81

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.
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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.
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PMID:Arachidonic acid causes postischemic dysfunction in control but not diabetic hearts. 210 41

Free radical activity has been implicated in the development of diabetic vascular complications in Type 1 diabetes. The aim of the present study was to investigate the levels of free radical scavengers, particularly erythrocyte superoxide dismutase, plasma and erythrocyte lysate thiol, and caeruloplasmin in 22 Type 2 diabetic patients clinically free of complications, and 15 comparable non-diabetic control subjects. The concentration (median (range] of both superoxide dismutase (23 (10-39) vs 45 (25-75) mumol l-1; p less than 0.001) and plasma thiol (374 (172-523) vs 460 (386-595) mumol l-1; p less than 0.01) were reduced in the diabetic group. There were no significant differences in the concentration of erythrocyte lysate thiol (199 (114-520) vs 188 (114-328) mumol l-1) or plasma caeruloplasmin (18 (9-31) vs 24 (6-50) mumol l-1) between the groups. This reduction in superoxide dismutase and the imbalance in the redox status of the plasma and lysate thiol demonstrated is consistent with an increase in free radical activity in Type 2 diabetes.
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PMID:Free radical activity in type 2 diabetes. 213 60

The great discovery by Furchgott of the relaxing factor released from the endothelium (EDRF) awakened us to the necessity to reevaluate the functional importance of endothelial cells that have been chemically or physically stimulated. EDRF was first demonstrated to be released by acetylcholine, substance P, bradykinin and calcium ionophore A23187; thereafter, many substances have been found to release EDRF. This factor is quite unstable, is not produced by cyclooxygenase, and is an activator of soluble guanylate cyclase that synthesizes cyclic GMP; its action is suppressed by antioxidants via the superoxide anions produced, potentiated by superoxide dismutase and abolished by methylene blue and oxyhemoglobin. Recently, the role of lipoxygenase products in the production of EDRF was evaluated with new 5-lipoxygenase inhibitors without antioxidant activity. During the last couple of years, the actions and chemical properties of EDRF were verified to be quite similar to those of nitric oxide (NO); therefore, the hypothesis of "EDRF = NO" is widely being accepted. NO is produced from L-arginine via catalysis by an enzyme that is activated by Ca2+. The enzyme activity is inhibited by L-monomethyl arginine and other L-arginine analogs. Chemical and physical stimulations increase intracellular Ca2+ in endothelial cells that seems to be associated with K(+)-channel opening and hyperpolarization. Current interests are directed to the possible roles of NO in the regulation of nerve function. There are evidences suggesting that NO modulates adrenergic nerve function in blood vessels and some brain cell functions regulated by cellular cyclic GMP. Particularly, NO may be a transmitter substance in non-adrenergic, non-cholinergic vasodilator nerves innervating the cerebral arteries. Future investigations will determine the physiological roles of EDRF or NO and its relationships to pathophysiology of vascular dysfunctions, such as vasospasm and those related to hypertension, diabetes, aging, etc., and the extended roles of NO in nerve function, inflammation, immune reactions, etc. would be clarified more extensively by accelerated progress in this field of research.
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PMID:[Endothelium-derived relaxing factor (EDRF)]. 216 93

Bactericidal ability of alveolar macrophages is depressed in rats with diabetes mellitus. To define the mechanism of this abnormality, we measured the parameters of respiratory burst in alveolar macrophages, peripheral blood monocytes, and neutrophils of rats 8 wk after the induction of diabetes by streptozocin. Superoxide anion (O2-.) generation during basal conditions and after stimulation with phorbol myristate acetate (PMA) was measured as superoxide dismutase-inhibitable cytochrome c reduction. NADPH, the principal substrate for NADPH-oxidase-dependent O2-. generation, was measured in the alveolar macrophages and quick-frozen lungs by the enzyme-cycling method. O2-. generation after PMA was significantly lower in the alveolar macrophages of diabetics than in the controls (14.4 +/- 2.0 nmol.10(6) cells-1.20 min-1 vs. 26.2 +/- 1.9, P less than 0.05). Conversely the peripheral blood monocytes of diabetics demonstrated an enhanced O2-. production after PMA stimulation. There was no significant difference in the neutrophil O2-.-generation between the groups. The alveolar macrophage NADPH (control 0.44 +/- 0.15 nmol/10(6) cells vs. diabetic 0.21 +/- 0.04, P less than 0.05) and lung tissue NADPH levels (control 81.4 +/- 16.3 nmol/g dry wt vs. diabetic 35.8 +/- 20.5, P less than 0.05) were significantly lower in the diabetics than in the controls. These data indicate that the O2-.-generating capacity of alveolar macrophages is markedly depressed in diabetes, whereas their precursors, monocytes, are primed to generate O2-. with PMA stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory burst in alveolar macrophages of diabetic rats. 216 35

Bepridil, a calcium antagonist with anti-anginal, anti-ischemic, and anti-arrhythmic properties was assessed for its ability to scavenge free radicals. Bepridil reduced the stable free radical 1,1-diphenyl-2-picrylhydrazil (DPPH) in the molar ratio 2:1 and, in this respect, was as active as the reference anti-oxidants hydroquinone and alpha-tocopherol. Allopurinol and SOD inhibited cytochrome c reduction in a hypoxanthine-xanthine oxidase superoxide generating system, whereas bepridil was ineffective. Deoxyribose degradation induced by the .OH radical was prevented by bepridil (IC50 = 0.050 mM). This ability to scavenge .OH was similar to that of dimethyl sulfoxide (DMSO) (IC50 = 0.056 mM) and more potent than that observed with mannitol and allopurinol (IC50 values of 0.74 mM and 0.92 mM, respectively). The powerful .OH scavenging activity of bepridil was confirmed in vivo on alloxan induced diabetes in mice. Bepridil exerted a marked protective effect at 0.150 mmol/kg whilst, ethanol and DMSO were active at the doses of 90 and 94 mmol/kg, respectively. These results demonstrate that bepridil is a potent .OH radical scavenger. This property may contribute to the therapeutic activity of this drug in myocardial ischaemia.
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PMID:Studies on the activity of bepridil as a scavenger of free radicals. 217 34

There is direct evidence that there is an increase of concentration of oxidizing species and oxidized products in plasma of human diabetics. The extent of this increase seems to reflect a predilection to diabetic damage. 1. A high concentration of lipid hydroperoxide in plasma was observed in diabetic patients and it's levels correlated well with the degree of diabetic nephropathy. 2. Lipid peroxide causes membrane injury of endothelial cells. The addition of anti-oxidant inhibited cell injury markedly. 3. Malondialdehyde and protein (lysin-residual or low density lipoprotein) made conjugates to change the antigenicity. This results shows the possibility that atherosclerosis as diabetic complication may be caused by immunological reactions with modified proteins for example, oxidized LDL and so on. 4. SOD activity in erythrocytes of diabetic patient was extremely decreased compared with non diabetics, but no difference was observed by the ELISA method with monoclonal antibody. Glycosylation had been expected to occur in various kinds of proteins. The inactivation of SOD may be caused by non enzymatic glycosylation, because negative correlation was observed between the activity of SOD and GHb in erythrocytes. This inactivation of SOD may play an important role in the pathogenesis of diabetic complications. From these results, it was suggested that both free radical reactions and non enzymatic glycosylation may play important roles not only in the development of diabetes but also in its complications.
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PMID:[Free radicals and diabetes mellitus]. 220 Sep 13

The basic and clinical studies that are expected to influence future laboratory medicine were presented by five speakers in the symposium held at the National Cardiovascular Center, in Osaka on January 27, 1990. Dr. Y. Katayama reported a new method for analyzing glycated protein by HPLC and the data on the positive error caused by superoxide anion in the value of fructosamine. Dr. Y. Harano described a sensitive method for enzyme immunoassay of apoprotein B and discussed cases of diabetes mellitus, hyperlipidaemia and hypo-apoprotein B with respect to the apoprotein B level. Dr. T. Noguchi reported the excellent results in DNA analysis of pyruvate kinase. Dr. N. Taniguchi presented a basic study on superoxide dismutase and noted the increased activity of this enzyme in certain diseases. The assay of this enzyme activity can now be routinely performed. Dr. H. Matsuo, the last speaker in this symposium, had received the Gakusiin award in 1989 for his studies on atrial natriuretic hormone (ANH). He outlined the history of ANH study developed in his laboratory. ANH also will be added to routine assay. We, the chairmen in this symposium, added comments concerning useful modern techniques for the clinical chemistry and the role of the clinical laboratory in large hospitals.
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PMID:[Progress in clinical chemistry]. 223 44

Superoxide dismutases (SOD) and their changes in diabetes, aging, ischemia and cancer were studied, Cu, Zn-SOD undergoes glycation reaction in vitro and in vivo and loses its activity by formation of Amadori compounds. Two lysine residues of Cu, Zn-SOD, Lys-122 and Lys-128 are primary glycated sites which are located on the surface of the molecule. The sites are also located on the active site liganding loop which plays a major role in the activity. The glycated Cu, Zn-SOD increased in the red cells of diabetic patients, especially those with diabetic complications. Mn-SOD appears in the serum of patients with acute myocardial infarction in a biphasic manner. The enzyme appears in sera 16 hr and 108 hr after the attack as determined by ELISA. The Mn-SOD levels are also increased in the serum of patients with epithelial ovarian cancer and it is a good marker for detecting and monitoring this cancer. Mn-SOD may play an important role in the ischemic and cancer tissues.
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PMID:[Superoxide dismutases: significances in aging, diabetes, ischemia and cancer]. 223 47


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