Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many individuals with cardiovascular diseases undergo periodic physical conditioning with or without medication. Therefore, this study investigated the interaction of exercise training and chronic nitroglycerin treatment on blood pressure (BP) and alterations in nitric oxide (NO), glutathione (GSH), antioxidant enzyme activities and lipid peroxidation in rats. Fisher 344 rats were divided into four groups: (1) sedentary control, (2) exercise training for 8 weeks, (3) nitroglycerin (15 mg/kg, s.c. for 8 weeks) and (4) training + nitroglycerin for 8 weeks. BP, heart rate (HR) and respiratory exchange ratio (RER) were monitored weekly for 8 weeks using tail-cuff method and oxygen/carbon dioxide analyzer, respectively. The animals were sacrificed 24 h after last treatments and plasma isolated and analyzed using HPLC, ELISA and UV-VIS spectrophotometric techniques. The results show that exercise conditioning significantly enhanced NO production (p < 0.001), GSH levels (p < 0.001), GSH/GSSG ratio (p < 0.05) and the up-regulation of the activities of catalase (CAT) (p < 0.05), glutathione peroxidase (GSH-Px) (p < 0.001), and glutathione reductase (GR) (p < 0.05), and depression of lactate levels (p < 0.001) in the plasma of the rat. These biochemical changes were accompanied by a significant increase in RER (p < 0.001) without a significant change in BP and HR. Chronic nitroglycerin administration significantly increased NO levels (p < 0.05), GSH levels (p < 0.001), superoxide dismutase (SOD) activity (p < 0.05), GST activity (p < 0.05), and decreased MDA levels (p < 0.05). These biochemical changes were accompanied by a significant decrease in BP (p < 0.05) and without any significant changes in HR and RER. Interaction of exercise training and chronic nitroglycerin treatment resulted in normalization of plasma NO, MDA, lactate levels, and CAT activity. The combination of exercise and nitroglycerin significantly enhanced GSH levels (p < 0.05), and the up-regulation of SOD (p < 0.001), GSH-Px (p < 0.05), GR (p < 0.05) and GST (p < 0.001) activities. These biochemical changes were accompanied by normalization of BP and a significant increased in RER (p < 0.001). The data suggest that the interaction of physical training and chronic nitroglycerin treatment resulted in the maintenance of BP and the up-regulation of plasma antioxidant enzyme activities and GSH levels in the rat.
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PMID:Interaction of physical training and chronic nitroglycerin treatment on blood pressure and plasma oxidant/antioxidant systems in rats. 1284 29

Nitric oxide (NO) is a short lived, readily diffusible intracellular messenger molecule associated with multiple organ-specific regulatory functions. In this communication, we elucidate the effect of exogenous NO administration, using nitroglycerin (GTN), on ferric nitrilotriacetate (Fe-NTA)-induced renal oxidative stress, hyperproliferative response and necrosis in ddY mice. Fe-NTA is a known complete renal carcinogen as well as renal and hepatic tumor promoter, which act by generating oxidative stress in the tissues. GTN treatment to ddY mice prior to Fe-NTA administration resulted in a highly significant protection against Fe-NTA-induced renal oxidative stress, hyperproliferative response and necrosis. In oxidative stress protection studies, the decrease in the level of renal glutathione and antioxidant enzyme activities induced by Fe-NTA were significantly reversed by GTN pretreatment in a dose-dependent manner (12-46% recovery, P<0.05-0.001). GTN pretreatment also resulted in a dose-dependent inhibition (24-39% inhibition, P<0.05-0.001) of Fe-NTA-induced lipid peroxidation as measured by TBARS formation in renal tissues. Similarly, in hyperproliferation protection studies, GTN pretreatment showed a strong inhibition of Fe-NTA-induced renal ornithine decarboxylase (ODC) activity (51-57% inhibition, P<0.001) and [3H]thymidine incorporation (43-58% inhibition, P<0.001) into renal DNA. GTN pretreatment almost completely prevented kidney biomolecules from oxidative damage and protected the tissue against the observed histopathological alterations. From this data, it can be concluded that exogenously produced NO from GTN might scavenge reactive oxygen species (ROS) and decreases toxic metabolites of Fe-NTA and thereby inhibiting renal oxidative stress. In addition, exogenously produced NO can also inhibit Fe-NTA-induced hyperproliferative response by down-regulating the activity of ODC and the rate of [3H]thymidine incorporation into renal DNA and could be suggested as another possible clinical application for this NO-donor (GTN, traditionally used as a vasodilator) in oncological medicine.
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PMID:Nitroglycerin, a nitric oxide generator attenuates ferric nitrilotriacetate-induced renal oxidative stress, hyperproliferative response and necrosis in ddY mice. 1457 7

Intravenous nitroglycerin (GTN) has been used as an anti-ischemic agent for the therapy of unstable and post-infarction angina. Nitric oxide (NO) and S-nitrosothiols constitute the biologically active species formed via nitroglycerin bioactivation. Increased levels of reactive oxygen species can diminish the therapeutic action of organic nitrates by scavenging donated NO and oxidizing tissue thiols important in nitrate biotransformation. Studies reported here show that the red cell activity of antioxidant enzymes, catalase and glutathione peroxidase, are significantly decreased after intravenous nitroglycerin treatment. Catalase activity (739.6 +/- 92.3 k/gHb) decreased to 440.1 +/- 111.9 and 459.8 +/- 130.7 k/gHb after 1 and 24 hr GTN infusion, respectively. Similarly, glutathione peroxidase activity (5.8 +/- 1.8 U/gHb) decreased to 3.2 +/- 1.7 and 3.8 +/- 1.1 U/g Hb after 1 and 24 hr GTN infusion, respectively. The reported decrease in antioxidant enzyme activities can lead to an oxidant milieu and contribute to the generation of nitrate tolerance.
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PMID:Effect of intravenous nitroglycerin therapy on erythrocyte antioxidant enzymes. 1611 1

Nanostructured lipid carriers (NLC) developed from mixtures of solid lipid and spatially incompatible liquid lipid by solvent diffusion method. This new type of lipid nanoparticles offers the advantage of improved drug loading capacity and release properties. In this study, Glyceryl distearate and Glyceryl behenate were chosen as solid lipid and Glyceryl triacetate used as liquid lipid. Ubidecarenone used as model drug was incorporated into the NLC. The influences of different type of solid lipid and liquid lipid concentration on physiochemical properties of the NLC were characterized. As a result, the drug encapsulation efficiencies were improved by adding the liquid lipid into the solid lipid of nanoparticles. NLC had higher encapsulation efficiency and drug release. In addition, in vivo study showed that the antioxidant activity of the Ubidecarenone (Co. Q10 NLC) was more effective than the Ubidecarenone (Coenzyme Q10) solution form on DPPH scavenging, anti-lipid peroxidation, lowers the effect of amnesia induced by scopolamine and increased bioavailability observed in Cmax, Tmax, and AUC. These results indicated that nanostructured lipid formulation of Ubiquinone (Coenzyme Q10) has more antioxidant activity than that of solution form and it can be used to reduce the oxidative stress and to increase the antioxidant enzyme activity in many neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease etc.
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PMID:Formulation and characterization of nanostructured lipid carrier of ubiquinone (Coenzyme Q10). 2362 Oct 1