UMLS:C0406810 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effect of melatonin on lipopolysaccharide (LPS)-induced oxidative damage in phenobarbital-treated rats was measured using the following parameters: changes in total glutathione (tGSH) concentration, levels of oxidized glutathione (GSSG), the activity of the antioxidant enzyme glutathione peroxidase (GSH-PX) in both brain and liver, and the content of cytochrome P450 reductase in liver. Melatonin was injected intraperitoneally (ip, 4mg/kg BW) every hour for 4 h after LPS administration; control animals received 4 injections of diluent. LPS was given (ip, 4 mg/kg) 6 h before the animals were killed. Prior to the LPS injection, animals were pretreated with phenobarbital (PB), a stimulator of cytochrome P450 reductase, at a dose 80 mg/kg BW ip for 3 consecutive days. One group of animals received LPS together with Nw-nitro-L-arginine methyl ester (L-NAME), a blocker of nitric oxide synthase (NOS) (for 4 days given in drinking water at a concentration of 50 mM). In liver, PB, in all groups, increased significantly both the concentration of tGSH and the activity of GSH-PX. When the animals were injected with LPS the levels of tGSH and GSSG were significantly higher compared with other groups while melatonin and L-NAME significantly enhanced tGSH when compared with that in the LPS-treated rats. Melatonin alone reduced GSSG levels and enhanced the activity of GSH-PX in LPS-treated animals. Additionally, LPS diminished the content of cytochrome P450 reductase with this effect being largely prevented by L-NAME administration. Melatonin did not change the content of P450 either in PB- or LPS-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Melatonin administration prevents lipopolysaccharide-induced oxidative damage in phenobarbital-treated animals. 759 65

Earlier studies have shown that inhibition of aggregation of washed platelets (WP) by NO was enhanced almost 100-fold by H2O2. In the present study, the interactions of H2O2 with nitrosothiols, the influence of the presence of plasma and the mechanism of the synergism were investigated. H2O2 strongly enhanced the inhibitory effects of S-nitrosoglutathione (GSNO) on thrombin-induced aggregation of WP. S-Nitrosoalbumin also inhibited platelets, and this was similarly enhanced by H2O2. The synergism with H2O2 was demonstrable for both exogenous GSNO and NO in the presence of plasma when platelets were stimulated with collagen. The inhibition of platelets by GSNO and H2O2 was completely inhibited by guanylate cyclase inhibitors. Synergism was also observed whether the H2O2 was added simultaneously or 1 min before or after the GSNO (or NO). This suggests that the action of H2O2 follows the occupation by NO of haem sites in guanylate cyclase and that a prior reaction between NO and H2O2 was not required. In the absence of exogenous GSNO or NO, H2O2 inhibited activation of platelets in plasma, an effect abolished by guanylate cyclase inhibitors. This suggested that endogenous NO donors in plasma or NO synthesized in platelets may interact with H2O2. Addition of NG-nitro-L-arginine methyl ester (hydrochloride) (L-NAME) decreased the effects of the H2O2 by 25%, indicating that the major endogenous source of NO in platelet-rich plasma was not derived from platelet synthesis of NO but from NO donors in plasma, such as nitrosothiols. Inhibition by H2O2 was also enhanced by beta-mercaptosuccinate, a glutathione peroxidase inhibitor that protects the H2O2. These results suggest a potent synergism of H2O2 with endogenous plasma nitrosothiols that inhibit platelet function through an intracellular mechanism involving guanylate cyclase.
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PMID:The synergism of hydrogen peroxide with plasma S-nitrosothiols in the inhibition of platelet activation. 883 16

Oxidative damage in various tissues of LPS-treated rats was studied using the following parameters: changes in reduced (GSH) and oxidized glutathione (GSSG) levels in liver, brain and lens; the activity of glutathione peroxidase (GSH-PX) in both liver and brain; the content of cytochrome P450 reductase in liver. Bacterial LPS was injected i.p. (at a dose of 4 mg/kg BW) 6 h before the animals were killed. One group of rats received N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS) (given for 4 days in the drinking water at a concentration of 50 mM); another group received both L-NAME and LPS. In brain and lens no changes in GSH were observed after either LPS, L-NAME or both. In contrast, GSSG and the GSSG/GSH ratio was significantly higher after LPS. This effect was abolished in the brain by L-NAME treatment. The level of the activity of the antioxidative enzyme GSH-PX in brain was significantly higher after L-NAME in LPS-treated animals. Hepatic GSH-PX activity was enhanced after either LPS, L-NAME or treatment with both substances. Additionally, LPS diminished the level of cytochrome P450 reductase with this effect being largely prevented by L-NAME. The results suggest that GSH, as an endogenous antioxidant, may play a major role in combating toxicity of LPS.
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PMID:Oxidative changes in the liver, brain and lens of lipopolysaccharide-treated rats. 884 34

In order to study effects of cigarette smoking and smoking cessation on plasma constituents and enzyme activities related to oxidative stress, 1255 smokers and 524 healthy non-smokers were investigated in terms of plasma levels of lipoperoxides (LPO), nitric oxide (NO), vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR). Additionally, erythrocytes were examined to determine the level of LPO, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). The results showed that, when compared with the average values of the non-smoker group, the average plasma values of LPO, NO and the average erythrocyte value of LPO in the smoker group were significantly increased (P < 0. 001), while the average plasma values of VC, VE, beta-CAR, and the average erythrocyte activities of SOD, CAT, GSH-Px were significantly decreased (P < 0.001). A linear regression and correlation analysis for 65 male smokers who were all 40 years old showed that with longer smoking duration and greater daily smoking quantity, the plasma values of LPO, NO and the erythrocyte value of LPO were elevated, while the plasma values of VC, VE, beta-CAR and erythrocyte values of SOD, CAT, GSH-Px were decreased. In a group of 73 smokers who stopped smoking completely for six months, the average plasma values of LPO, NO and the average erythrocyte value of LPO decreased, although they were still significantly higher than those in the matched non-smoker group (P < 0.05). Additionally, the average plasma values of VC, VE, beta-CAR and the average erythrocyte values of SOD, CAT, GSH-Px increased, although they were still significantly lower than those in the matched non-smoker group (P < 0.05). However, after smoking cessation for one year the above average values were not significantly different from those in the matched non-smoker group (P > 0.05). This finding indicates that the markedly increased oxidative stress in smokers might gradually return to normal but only after a long period of smoking cessation. In conclusion, in the bodies of smokers a series of free radical chain reactions were gravely aggravated, the dynamic balance between oxidation and antioxidation was seriously disrupted, and oxidative stress was clearly exacerbated, which is closely related to many disorders or diseases in smokers. The present study underscored the need, urgency and importance of complete smoking cessation.
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PMID:Effects of cigarette smoking and smoking cessation on plasma constituents and enzyme activities related to oxidative stress. 1085 40

Hemodynamic forces have profound effects on vasculature. Laminar shear stress upregulates superoxide dismutase (SOD) expression in endothelial cells. SOD converts superoxide anion to H(2)O(2), which, however, promotes atherosclerosis. Therefore, defense against H(2)O(2) may be crucial in reducing oxidative stress. Since glutathione peroxidase (GPx-1) reduces H(2)O(2) to H(2)O, the regulation of GPx-1 expression by mechanical stress was examined. Cultured bovine aortic endothelial cells (BAECs) were subjected to laminar shear stress and stretch force. Shear stress upregulated GPx-1 mRNA expression in a time- and force-dependent manner in BAECs, whereas stretch force was without effect. Furthermore, shear stress increased GPx activity. L-NAME, an inhibitor of nitric oxide synthase, did not affect shear stress-induced GPx-1 mRNA expression. The ability of laminar shear stress to induce GPx-1 expression in endothelial cells may be an important mechanism whereby shear stress protects vascular cells against oxidative stress.
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PMID:Shear stress enhances glutathione peroxidase expression in endothelial cells. 1087 65

Protective effects of NOS inhibitors and free radical scavengers in cerebral ischemia are well documented. The present study was undertaken to determine the possible effects of NOS inhibition on brain antioxidants. Levels of both enzymatic [glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD)] and non-enzymatic [reduced glutathione (GSH)] antioxidants following nitric oxide synthase (NOS) inhibition by N(G)-nitro-L-arginine methyl ester (L-NAME), D-NAME or 7-nitroindazole (7-NI) have been investigated. NOS activity and antioxidant levels in the rat cerebellum and medulla were estimated 1 h after treatment with L-NAME (10, 30 and 100 mg/kg, i.p.), D-NAME (100 mg/kg, i.p.) or 7-NI (25 mg/kg, i.p.). L-NAME and 7-NI inhibited NOS activity in a dose-dependent manner. D-NAME also exhibited significant NOS inhibition. The activity of SOD and the GSH level remained unaltered following NOS inhibition. However, L-NAME and D-NAME at 100 mg/kg attenuated GPx activity in the cerebellum, though 7-NI had no effect. L-NAME inhibited catalase activity in medulla only at 30 mg/kg, but had no effect in cerebellum. However, 7-NI (25 mg/kg), D-NAME and L-NAME at 100 mg/kg did not affect catalase activity in the rat brain. Thus, NOS inhibition by the three agents did not have major effects on brain antioxidant levels.
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PMID:Antioxidant levels in the rat brain after nitric oxide synthase inhibition: a preliminary report. 1093 75

To further reveal the risks of heroin abuse to human body, and to determine the injuries of oxidation, peroxidation and lipoperoxidation induced by nitric oxide and other free radicals to heroin abusers, we determined and compared plasma values of lipoperoxides (LPO), nitric oxide (NO), vitamin C (VC), vitamin E (VE), beta-carotene (beta-CAR) and erythrocyte values of LPO, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in 114 heroin abusers and 100 healthy volunteers. Using linear regression and correlation as well as stepwise regression and correlation, we also analyzed the effect of the abusing duration, and daily abusing quantity on the above-mentioned biochemical parameters in the heroin abusers. The results showed that, compared with the healthy volunteer groups, the average plasma values of LPO, and NO, and the average erythrocyte value of LPO in the heroin abuser group were significantly increased (P < 0.0001), and the average plasma values of VC, VE, and beta-CAR and the average erythrocyte values of SOD, CAT, and GSH-Px were significantly decreased (P < 0.0001). Analysis of linear regression and correlation showed that with prolonged heroin abusing and with increased daily quantity in the heroin abusers, the plasma values of LPO, and NO, and the erythrocyte value of LPO were gradually increased (P < 0.001), whereas the plasma values of VC, VE, and beta-CAR and the erythrocyte values of SOD, CAT, and GSH-Px were gradually decreased (P < 0.001). Analysis of stepwise regression and correlation indicated that the plasma values of NO, VC and VE were closely correlated with the abusing duration and daily abusing quantity. These results indicate that the balance between oxidation and antioxidation in the heroin abusers was seriously disturbed, and the injuries induced by nitric oxide and other free radicals, through oxidation, peroxidation and lipoperoxidation to the bodies of heroin abusers exacerbated. It is therefore necessary that in abstaining from heroin dependence, the heroin abusers should acquire sufficient quantities of antioxidants such as VC, VE and beta-CAR.
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PMID:Heroin abuse and nitric oxide, oxidation, peroxidation, lipoperoxidation. 1105 15

Diesel exhaust particles (DEP) have been proved to induce serious pulmonary injury, among which lethal pulmonary edema has been assumed to be mediated by vascular endothelial cell damage. In the present study, we investigated the cytotoxic mechanism of DEP on human pulmonary artery endothelial cells focusing on the role of active oxygen species. Endothelial cell viability was assessed by WST-8, a novel tetrazolium salt. Nitric oxide (NO) production was measured by using a new fluorescence indicator, diaminofluorescein-2 (DAF-2). Organic compounds in DEP were extracted by dichloromethane and methanol. DEP-extracts damaged endothelial cells under both subconfluent and confluent conditions. The DEP-extract-induced cytotoxicity was markedly reduced by treatment with SOD, catalase, N-(2-mercaptopropionyl)-glycine (MPG), or ebselen (a selenium-containing compound with glutathione peroxidase-like activity). Thus superoxide, hydrogen peroxide, and other oxygen-derived free radicals are likely to be implicated in DEP-extract-induced endothelial cell damage. Moreover, L-NAME and L-NMA, inhibitors of NO synthase, also attenuated DEP-extract-induced cytotoxicity, while sepiapterin, the precursor of tetrahydrobiopterin (BH(4), a NO synthase cofactor) interestingly enhanced DEP-extract-induced cell damage. These findings suggest that NO is also involved in DEP-extract-mediated cytotoxicity, which was confirmed by direct measurement of NO production. These active oxygen species, including peroxynitrite, may explain the mechanism of endothelial cell damage upon DEP exposure during the early stage.
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PMID:The cytotoxic effects of diesel exhaust particles on human pulmonary artery endothelial cells in vitro: role of active oxygen species. 1118 26

To study the relationship of oxidative, antioxidative constituents and antioxidases in blood with chronic cholecystitis containing gallstone, levels of lipoperoxides (LPO), nitric oxide (NO), vitamin C(VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as level of LPO, activities of superoxide dismulase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) in erythrocytes were investigated by spectrophotometric assay in 107 patients with this condition (PCg) and 100 healthy volunteers (HVs). Compared with HVs group, the average value of LPO and NO in plasma and that of LPO in erythrocytes of PCg group were significantly increased (P < 0.0001), while that of VC, VE and beta-CAR in plasma and the average activities of SOD, CAT and GSH-Px in erythrocytes were significantly decreased (P < 0.0001). Linear regression and correlation analysis for 107 preoperative PCg showed that the value of LPO and NO in plasma and that of LPO in erythrocytes of PCg gradually increased (P < 0.0001), representing a significant linear positive correlation. The value of VC, VE and beta-CAR in plasma and that of SOD, CAT and GSH-Px in erythrocytes of PCg gradually decreased (P < 0.0001), representing a significant linear negative correlation. Stepwise regression and correlation analysis for 107 preoperative PCg suggested that the closest correlation was observed between the course of disease and the value of NO and VC in plasma and that of SOD, GSH-Px and LPO in erythrocytes, r = 0.7306, F = 32.1408, P < 0.0001. Compared with the preoperative PCg group, the average value of LPO and NO in plasma and that of LPO in erythrocytes of the postoperative PCg group were significantly decreased (P < 0.0001). Furthermore, the average value of VC in plasma and that of SOD, CAT and GSH-Px in erythrocytes of the postoperative PCg group were significantly increased (P < 0.0001), whereas no significant difference was found between their average value of VE and beta-CAR in plasma. These findings suggested that oxidative stress was an aggravating pathological condition in PCg group. Therefore, we recommend that in treating PCg, antioxidants such as VC, VE, beta-CAR should be given in order to alleviate their potential oxidative damages.
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PMID:Oxidative stress before and after operation in patients with chronic cholecystitis containing gallstone. 1135 58

Plasma vitamin C(P-VC), vitamin E(P-VE) and beta-carotene(P-beta-CAR) contents and the activities of superoxide dismutase(E-SOD), catalase(E-CAT) and glutathione peroxidase (E-GSH-Px) in erythrocyte in 73 silicosis patients and 60 healthy control subjects were measured. The average levels of P-VC, P-VE, P-beta-CAR, E-SOD, E-CAT and E-GSH-Px of patients were significantly lower than those of the controls (P < 0.001). All indexes were correlated to the course, condition and pulmonary function of silicosis patients. The results analyzed by stepwise regression showed that the correlation between course, condition and pulmonary function of patients and P-VE and E-SOD was close. The balance between oxidation and the antioxidation in silicosis patients may be disturbed, and oxygen free radical reaction may be pathologically exacerbated.
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PMID:[Study on the correlation of silicosis with antioxidant and antioxidase]. 1193 4

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