Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of chronic adriamycin treatment on cellular defence mechanisms against free radicals has been determined in rats. To that end, the changes in vitamin E content, activity of superoxide dismutase, catalase and factors of the glutathione system were measured in heart, kidneys and liver after 24 and 52 days of treatment. Moreover, damage was assessed by measuring the activity of NADPH- and NADH-cytochrome c reductase. The results concerning the components of the oxidative defence systems in male rats showed reductions in the activity of superoxide dismutase and catalase in renal tissue and in factors of the glutathione system in liver tissue. In cardiac tissue an increased activity of catalase and elevated content of total glutathione were found. Vitamin E content was increased in liver and to a lesser extent, in kidneys. The activity of Se-dependent glutathione peroxidase sharply decreased only in liver. Major differences between male and female rats were not observed in renal and cardiac tissue, as far as protective factors were concerned. However, a decrease in catalase activity was detectable earlier in male kidneys. The protective factors in liver of female rats were far less susceptible to in vivo treatment with adriamycin, as compared to liver of male rats. Decreased activity of the cytochrome reductases was found in liver of male rats. In male renal tissue only cytochrome c reductase activity was significantly reduced. Male cardiac tissue showed no signs of biochemical damage, although from histological examination in a parallel study [J Natl Cancer Inst 76: 299-307 (1986)] lesions were evident. In female rats no damage was found in liver, kidneys and heart.
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PMID:The effect of chronic adriamycin treatment on heart kidney and liver tissue of male and female rat. 337 82

The effect of iron-overload on rat kidney was studied after a single injection of iron-dextran. Total iron content in kidney and isolated kidney mitochondria was markedly elevated over control values. To assess mitochondrial damage by iron overload, succinate-cytochrome c reductase and NADH-cytochrome c reductase activities as well as the rate of succinate-dependent hydrogen peroxide generation were measured. None of these activities were significantly affected by acute iron overload. The net content and the rate of TBARS (thiobarbituric acid reactive species) formation in kidney homogenates from iron-treated rats was significantly higher than that of control animals. Total superoxide dismutase activity in the homogenates from iron overloaded kidney was decreased by 26%, as compared to controls. Catalase, glutathione peroxidase, and Mn-superoxide dismutase activities were not affected by the treatment. The content of alpha-tocopherol was consistently decreased in whole kidney homogenates (-31%), mitochondria from kidney medulla (-31%) and cortex (-34%), from iron-overloaded rats. Our data suggest that iron dextran treatment does not affect kidney integrity, even though increases in lipid peroxidation occur. Vitamin E appears to be effective in controlling iron-dextran dependent radical generation in kidney.
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PMID:Resistance of rat kidney mitochondrial membranes to oxidation induced by acute iron overload. 816 Jan 95

Vitamin E, the major lipid chain-breaking antioxidant in erythrocyte membranes, is present in low concentration, suggesting that mechanisms should exist to protect against its loss. Enzymatic pathways for the recycling of vitamin E from its tocopheroxyl radical have been observed previously in inner membranes of mitochondria and microsomes. These pathways use electron transport enzymes and their substrates to regenerate vitamin E. Erythrocyte membranes also contain significant NADH-cytochrome c reductase activity, as well as cytochrome b5, the function of which is not yet known. Using an enzymatic oxidation system composed of lipoxygenase and arachidonic acid, free radicals were produced in human erythrocyte membranes, and their reaction with chromanols was followed by ESR and high performance liquid chromatography (HPLC). Since the endogenous vitamin E content of the membranes is very low, we used a vitamin E homologue lacking the hydrocarbon chain (2,2,5,7,8-pentamethyl-6-hydroxychromane) as a probe molecule for ESR measurements. However, parallel HPLC determinations of lipid hydroperoxides and of endogenous vitamin E confirmed the results obtained by ESR. It was found that protection against the loss of vitamin E can be provided either by NADH-cytochrome b5-dependent enzymatic recycling or by a nonenzymatic pathway involving ascorbate and dihydrolipoic acid.
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PMID:Vitamin E recycling in human erythrocyte membranes. 838 77

Male mice receiving vitamin E (5.0 g alpha-tocopherol acetate/kg of food) from 28 wk of age showed a 40% increased median life span, from 61 +/- 4 wk to 85 +/- 4 wk, and 17% increased maximal life span, whereas female mice equally supplemented exhibited only 14% increased median life span. The alpha-tocopherol content of brain and liver was 2.5-times and 7-times increased in male mice, respectively. Vitamin E-supplemented male mice showed a better performance in the tight-rope (neuromuscular function) and the T-maze (exploratory activity) tests with improvements of 9-24% at 52 wk and of 28-45% at 78 wk. The rates of electron transfer in brain mitochondria, determined as state 3 oxygen uptake and as NADH-cytochrome c reductase and cytochrome oxidase activities, were 16-25% and 35-38% diminished at 52-78 wk. These losses of mitochondrial function were ameliorated by vitamin E supplementation by 37-56% and by 60-66% at the two time points considered. The activities of mitochondrial nitric oxide synthase and Mn-SOD decreased 28-67% upon aging and these effects were partially (41-68%) prevented by vitamin E treatment. Liver mitochondrial activities showed similar effects of aging and of vitamin E supplementation, although less marked. Brain mitochondrial enzymatic activities correlated negatively with the mitochondrial content of protein and lipid oxidation products (r2 = 0.58-0.99, P < 0.01), and the rates of respiration and of complex I and IV activities correlated positively (r2 = 0.74-0.80, P < 0.01) with success in the behavioral tests and with maximal life span.
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PMID:Vitamin E at high doses improves survival, neurological performance, and brain mitochondrial function in aging male mice. 1602 May 19

We investigated the effects of chronic administration of vitamin E on nitric oxide (NO)-producing neurons in the brains of streptozotocin (STZ)-induced diabetic rats using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. We further evaluated the effects of diabetes and vitamin E treatment on experimental anxiety and memory processes using the elevated plus maze (EPM) Trial 1/2 protocol. Wistar rats were divided into four groups: normoglycemics (N), normoglycemics treated with vitamin E (NVE), diabetics (D), and diabetics treated with vitamin E (DVE). Diabetes mellitus was induced by a single intraperitoneal injection of STZ (35mg/kg). Vitamin E (100mg/kg) or vehicle was administered orally by gavage (1ml/kg) once each day for 7 weeks. After behavioral testing, the dentate gyrus of the hippocampus (DG), striatum, paraventricular nucleus of the hypothalamus (PVN), supraoptic nucleus (SON), and dorsolateral periaqueductal grey (DLPAG) were analyzed for NADPH-d histochemistry. STZ-induced diabetic rats exhibited decreased locomotor activity and cognitive impairment compared with normoglycemic controls. The number of NADPH-d-positive neurons was increased in the DG, striatum, and DLPAG of diabetic rats. An increase in soma area was detected in all structures analyzed (DG, striatum, PVN, SON, and DLPAG) of STZ-induced diabetic animals. The present study showed that chronic administration of vitamin E ameliorates memory in STZ-induced diabetic rats and revealed that NOS-producing neurons have an increased soma area which can be restored, at least partially, by vitamin E treatment. These results suggest the potential use of vitamin E as an adjuvant therapy for the prevention and treatment of diabetic conditions.
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PMID:Vitamin E improves learning performance and changes the expression of nitric oxide-producing neurons in the brains of diabetic rats. 2013 20

The present study has been designed to explore the nitric oxide mechanism in the protective effect of desipramine, venlafaxine and trazodone against I/R induced oxidative stress and mitochondrial dysfunction in mice. Vitamin E was taken as standard antioxidant. Laca mice (25-30 g) were subjected to twice BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. The drug treatments were started from the day of surgery and continued for the next four days. After 96 h the animals were sacrificed for biochemical (malondialdehyde, nitrite concentration, superoxidedismutase, catalase, redox ratio and GST) and mitochondrial enzyme complex (NADH dehydrogenase, succinate dehydrogenase, MTT assay and cytochrome c oxidase) estimations. Ischemia caused significant oxidative damage and mitochondrial enzyme dysfunction after 96 h of reperfusion as compared to sham operated animals. Antidepressant (desipramine, venlafaxine and trazodone) treatment significantly attenuated oxidative damage and restored mitochondrial enzyme complex activities as compared to control (I/R) group. Further, protective effects of desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) were attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with desipramine (15 mg/kg) and/or venlafaxine (5 mg/kg) significantly potentiated their protective effect which was significant as compared to their effect alone. The present study highlights the involvement of nitric oxide mechanism in the protective effects of desipramine and venlafaxine against I/R induced oxidative stress and mitochondrial dysfunction in mice.
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PMID:Protective effect of desipramine, venlafaxine and trazodone against experimental animal model of transient global ischemia: possible involvement of NO-cGMP pathway. 2062 74