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)

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

In this study it was of interest to evaluate the impact of nitric oxide (NO) modulation by administration of arginine/NAME, on oxidative stress in experimental colitis induced by 2,4,6-trinitrobenzenesulfonic acid. Arginine was used to increase NO levels while NAME lowered oxidant levels. Histopathological findings of colon revealed mucosal inflammation in all groups but significantly higher with arginine alone. The levels of NO and of thiobarbituric acid-reactive substances (TBARS, a marker of lipid peroxidation) were observed to be significantly higher in the arginine-administered group compared to glycine, and these levels were found to decrease on administration of NAME to both glycine- and L-arginine-administered groups. Glutathione peroxidase (GSH-Px) activity and glutathione (GSH) levels were significantly higher in arginine administered group compared to glycine. Significantly higher CuZn superoxide dismutase (CuZn-SOD) activity was observed in the L-arginine + L-NAME group compared to arginine. Data show that NO plays a role in oxidant damage found in experimental colitis and that the use of NAME may potentially inhibit injury.
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PMID:Evaluation of oxidative stress in experimental colitis: effects of L-arginine-nitric oxide pathway manipulation. 1103 5

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

The present study investigated the effect of nitric oxide (NO) on the lifespan of the corpus luteum (CL). Using a competitive nitric oxide synthase (NOS) inhibitor, L-nitro arginine methyl ester (L-NAME, 600 micromol/l), and a long-life NO donor, diethyl-aminetriamine (DETA-NONOate, 10(-8), 10(-6) or 10(-4) mol/l), we found that in ovaries from rats at the mid stage of CL development, endogenous NO increased both glutathione (GSH) and progesterone production. However, during prostaglandin F(2 alpha) (PGF(2 alpha))-induced luteolysis NO acted as an intermediary molecule in the inhibitory effect of PGF(2 alpha), on GSH content. This was supported by the fact that in-vivo PGF(2 alpha) treatment enhanced nitric oxide synthase (NOS) activity. These results indicate that the NO could act with a dual action (protective or pro-oxidant) in CL development.
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PMID:Dual effects of nitric oxide in functional and regressing rat corpus luteum. 1113 59

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

The present study aims at investigating the role of nitric oxide (NO) on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion (I/R) and its relation to mucus. NO synthesis modulators such as L-arginine and N(G)-nitro-L-arginine methyl ester (L-NAME) were injected intraperitoneally to the rats 30 min prior to I/R which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. As a result, I/R increased lipid peroxide production and decreased the contents of glutathione (GSH), cGMP and mucus as well as GSH peroxidase activities of gastric mucosa. I/R decreased the activity and protein of NO synthase (NOS) in gastric mucosa. Pretreatment of L-arginine, a substrate for NOS, prevented I/R-induced alterations of gastric mucosa. However, L-NAME, an NOS inhibitor, deteriorated oxidative damage induced by I/R. In conclusion, NO has an antioxidant defensive role on gastric mucosa by maintaining mucus, GSH and GSH peroxidase, which were related to preservation of cGMP and NOS in gastric mucosa.
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PMID:Role of nitric oxide and mucus in ischemia/reperfusion-induced gastric mucosal injury in rats. 1135 95

The aim of the present study was to investigate the underlying mechanism of the role of hot water extract of black tea [Camellia sinensis (L). O. Kuntze Theaceae] in normalizing the changes in intestinal transit and gastric emptying induced by various ulcerogenic agents in experimental rats. Intestinal transit as well as gastric emptying were significantly reduced in rats treated with glutathione (GSH) depleting agents, diethyl maleate (DEM), indoacetamide (IDA) and N-ethyl maleimide (NEM). Prior oral administration of black tea extract (BTE) at 20 ml/kg of a 10% solution, i.g. once a day for 7 days significantly increased the intestinal transit and gastric emptying with restoration of serum GSH level. Singular administration of succimer (60 mg/kg, i.g.), the standard sulfhydryl containing antiulcer agent used as a reference drug, was also effective. Increase in intestinal transit caused by BTE was reversed both by N-omega-nitro-L-arginine methyl ester (L-NAME) (25 mg/kg, i.p.) and N-omega-monomethyl-L-arginine (L-NMMA) (25 mg/kg, i.p.), but not with N-omega-nitro-D-arginine methyl ester (D-NAME) (25 mg/kg, i.p.). Furthermore, restoration of intestinal nitric oxide synthase (NOS) activity was found to be associated with BTE treatment. These results provide evidence that nitric oxide may play a role in BTE-mediated improvement of intestinal motility changes and gastric emptying induced by DEM, IDA and NEM.
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PMID:Role of reduced glutathione and nitric oxide in the black tea extract-mediated protection against ulcerogen-induced changes in motility and gastric emptying in rats. 1138 38

The ubiquitin/proteasome pathway plays an essential role in protein turnover in vivo, and contributes to removal of oxidatively damaged proteins. We examined the effects of proteasome inhibition on viability, oxidative damage and antioxidant defences in NT-2 and SK-N-MC cell lines. The selective proteasome inhibitor, lactacystin (1 microM) caused little loss of viability, but led to significant increases in levels of oxidative protein damage (measured as protein carbonyls), ubiquitinated proteins, lipid peroxidation and 3-nitrotyrosine, a biomarker of the attack of reactive nitrogen species (such as peroxynitrite, ONOO(-)) upon proteins. Higher levels (25 microM) of lactacystin did not further increase the levels of carbonyls, lipid peroxidation, 3-nitrotyrosine, or ubiquitinated proteins, but produced increases in the levels of 8-hydroxyguanine (a biomarker of oxidative DNA damage) and falls in levels of GSH. Lactacystin (25 microM) caused loss of viability, apparently by apoptosis, and also increased production of nitric oxide (NO.) (measured as levels of NO2- plus NO3-) by the cells; this was inhibited by N-nitro-L-arginine methyl ester (L-NAME), which also decreased cell death induced by 25 microM lactacystin and decreased levels of 3-nitrotyrosine. The NO. production appeared to involve nNOS; iNOS or eNOS were not detectable in either cell type. Another proteasome inhibitor, epoxomicin, had similar effects.
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PMID:Effect of proteasome inhibition on cellular oxidative damage, antioxidant defences and nitric oxide production. 1143 71

Primary cultures of hepatocytes are a widely used in vitro model for biochemical research. Following isolation, hepatocytes produce large amounts of nitric oxide (NO), which is known to have both pro- and anti-apoptotic effects in hepatocytes in vivo and in vitro. Previous work has not determined the effect of these increased levels of NO on the response of hepatocytes to apoptotic stimuli. Here we report that levels of nitrites are elevated in hepatocyte monolayers from 24 h onwards. Addition of the inducible nitric oxide synthase (iNOS) inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), to the medium inhibited this increase in nitrites. These results indicate that the increase in nitrite is most likely due to the formation of NO. Elevated nitrite levels had no effect either on basal levels of apoptosis or on ATP and GSH. Apoptosis was induced by transforming growth factor beta-1 (TGFbeta-1) or glycochenodeoxycholate (GCDC). Both compounds caused moderate hepatocyte apoptosis; however, addition of L-NAME prior to exposure significantly increased the level of apoptosis observed with the two compounds. Both TGFbeta-1 and GCDC had no effect on hepatocyte ATP or GSH levels; however, as a consequence of secondary necrosis, TGFbeta-1 exposure significantly increased levels of lactate dehydrogenase (LDH) leakage. These findings indicate that the increased levels of NO associated with the culture of hepatocytes have an inhibitory effect on compound-induced apoptosis in the cells.
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PMID:Spontaneous nitric oxide in hepatocyte monolayers and inhibition of compound-induced apoptosis. 1169 61

Oxygen free radicals are implicated in the pathophysiology of ischemia-reperfusion (I/R) injury in skeletal muscle. Nitric oxide (NO) and prostaglandin E2 (PGE2) are important regulators of the microcirculation in skeletal muscle. The effects of L-arginine, substrate for NO, and N(G)-nitro L-arginine methyl ester (L-NAME) on PGE2 synthesis, lipid peroxidation and reduced glutathione (GSH) levels was investigated in the rat gastrocnemius muscle after 3 h of reperfusion following 2 h of ischemia. Lipid peroxidation and GSH levels showed a non-significant changes in the I/R groups compared to the control group. According to these results, it can be assumed that skeletal muscle can resist 2 h of ischemia followed by 3 h of reperfusion-induced oxidative stress. PGE2-like activity in the gastrocnemius muscle increased in the L-NAME treated and I/R groups. L-arginine administration reversed the increase in PGE2-like activity of reperfused skeletal muscle. These findings support the conclusion that endothelium-derived PGE2 synthesis increases during reperfusion and suggest that PGE2 may have a protective role in the maintenance of endothelial function.
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PMID:Effects of nitric oxide donor and inhibitor on prostaglandin E2-like activity, malondialdehyde and reduced glutathione levels after skeletal muscle ischemia-reperfusion. 1172 69


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