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

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

Hydra feeding response is a very primitive olfactory-like behavior present in a multicellular organism. We investigated the role of nitric oxide (NO) in the induction and control of hydra feeding response. Under basal conditions, hydra specimens produce detectable amounts of nitrite (NO2-), the breakdown product of NO. When hydra were incubated with reduced glutathione (GSH), the typical activator of feeding response, an increase of basal NO production was observed. This effect was inhibited by glutamic or alpha-aminoadipic acids, two GSH antagonists, which block GSH-induced feeding response, and by the NO synthase (NOS) inhibitor L-NAME. Moreover, we found that hydra possess a calcium-dependent (but calmodulin-independent) NOS isoform. By using exogenous NO donors and NOS inhibitors, we demonstrated that NO stimulus can participate both in triggering tentacular movements and in recruiting neighbor tentacles during hydra feeding response. By using dbt2-cGMP, an analog to cGMP, we observed that the NO effect was independent of cGMP pathway. Our results strongly implicate NO involvement in hydra very primitive feeding behavior, thus confirming its preservation throughout evolution.
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PMID:Nitric oxide involvement in Hydra vulgaris very primitive olfactory-like system. 898 73

The purpose of this study was to characterize the protective effect of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, on oxidative stress-induced endothelial cell injury. Intracellular oxidative stress was induced by 1-chloro-2,4-dinitrobenzene, a glutathione (GSH) depleting agent, and the leakage of intracellular lactate dehydrogenase was measured as a marker of cell injury. Addition of 1-chloro-2,4-dinitrobenzene (100-500 microM) induced leakage of lactate dehydrogenase from endothelial cells, and the leakage of lactate dehydrogenase was strongly attenuated by L-NAME, but not by NG-methyl-L-arginine, also an inhibitor of nitric oxide synthase. However, cell injury induced by the Ca2+ ionophore ionomycin was not affected by L-NAME or NG-methyl-L-arginine. Moreover, neither L-NAME nor NG-methyl-L-arginine affected GSH depleting agent-induced or H2O2-induced cell injury in a rat foetal lung fibroblast cell line which lacks nitric oxide synthase. These results suggest that the protective effect of L-NAME is likely to be related to nitric oxide synthase, while the inhibition of nitric oxide production may not be involved in the protective effect of L-NAME, since NG-methyl-L-arginine did not affect endothelial cell injury.
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PMID:Possible involvement of nitric oxide synthase in oxidative stress-induced endothelial cell injury. 914 Jan 39

Oxidative stress may contribute to nigral cell death in Parkinson's disease based on postmortem investigations showing increased iron levels, decreased levels of reduced glutathione (GSH), and impaired mitochondrial function. This leads to oxidative damage because lipid peroxidation is increased in substantia nigra and there is a widespread increase in protein and DNA oxidation in the brain in Parkinson's disease. Nitric oxide (NO) may be one of the free radical species involved in nigral degeneration. NO is involved in the production of hydroxyl radicals resulting from MPP+-induced dopamine efflux in striatum. Mice treated with the neuronal nitric oxide synthase (NOS) inhibitor 7-nitroindazole show reduced toxicity to MPTP and knock-out mice lacking neuronal NOS show decreased MPTP susceptibility. In primates, 7-nitroindazole inhibits MPTP toxicity but this remains controversial because no protection is afforded by the nonspecific NOS inhibitor, L-NAME. Indeed, in Parkinson's disease itself, there is little evidence for nitric oxide's involvement in nigral pathology. A susceptibility factor for the development of Parkinson's disease may involve isoforms of cytochrome P450, some of which are found in the brain. CYP2EI, which is associated with free radical production and the formation of endogenous toxins, is selectively localized in nigral dopamine-containing cells. CYP2E1 metabolizes n-hexane leading to the formation of its neurotoxic metabolite 2,5-hexanedione which may explain cases of solvent-induced parkinsonism. Oxidative processes clearly contribute to the pathology of Parkinson's disease but are probably secondary to some other primary unidentified cause, presumably genetic or environmental. Nevertheless, their involvement may allow therapeutic intervention in the cascade of events associated with the progression of Parkinson's disease.
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PMID:Oxidative mechanisms in nigral cell death in Parkinson's disease. 961 15

The present study aims at investigating the effects of nitric oxide (NO) on hydrogen peroxide (H2O2)-induced damage in isolated rabbit gastric glands. NO synthesis modulators such as L-arginine and NG-nitro-L-arginine methyl ester (L-NAME) and an NO donor, sodium nitroprusside, were added to isolated rabbit gastric glands exposed to H2O2, generated by glucose oxidase acting on beta-D-glucose. As a result, glucose/glucose oxidase caused an increase in lipid peroxide production and decreases in reduced glutathione (GSH) content, GSH peroxidase activity, nitrite release, and mucus secretion in gastric glands. The alterations in lipid peroxide production, GSH content, and mucus secretion were prevented by pretreatment with L-arginine, a substrate for NO synthase and sodium nitroprusside, but not by L-NAME. In conclusion, NO protects gastric glands from H2O2 by inhibiting lipid peroxidation and maintaining cellular GSH content and mucus secretion.
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PMID:Effect of nitric oxide on hydrogen peroxide-induced damage in isolated rabbit gastric glands. 979 73

A dual role for nitric oxide (NO) in ischemia-reperfusion (I/R) injury is still controversial. This study aims to investigate the role of NO in rat hepatic reperfusion injury. Ischemia was induced by total occlusion of hepatic artery and portal vein for 30 min, then the tissue was reperfused for 30 min. The animals in the L-NAME group (n=10) received N(G)nitro-L-arginine methyl ester (L-NAME) (15 mg/kg) intraperitoneally 60 min before ischemia. The ischemia group (n=10) was given an equal volume of saline solution. The control group comprised eight healthy rats which were not exposed to ischemia or reperfusion. An indicator of hepatic injury, plasma alanine amino transferase (ALT) enzyme activities, were increased in the L-NAME group as compared with the ischemia group (p<0.001). The level of serum nitrite, an index of NO production, and hepatic reduced glutathione (GSH) concentration were lower in the L-NAME group than in the ischemia group (p<0.001, p<0.01, respectively). Hepatic levels of malondialdehyde (MDA) and conjugated dienes (CD) were significantly increased in the L-NAME group as compared to the ischemia group (p<0.05, p<0.001, respectively). Our results confirm that L-NAME, an inhibitor of the enzyme NO synthase, increased the lipid peroxidation and possibly tissue injury, due to the inhibition of cytoprotective effects of NO in a rat hepatic I/R model.
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PMID:The effect of nitric oxide on ischemia-reperfusion injury in rat liver. 1052 58

Nitric oxide (NO) is a short-lived, readily diffusible intracellular messenger molecule associated with multiple organ-specific regulatory functions. Endogenous stimulation or exogenous administration of NO have been shown to inhibit production of reactive oxygen species (ROS) and expression of oxidant-mediated molecular or tissue injury. Potassium bromate (KBrO3) is one such potent renal oxidant that acts through generation of ROS-mediated lipid peroxidation, and causes increased ornithine decarboxylase activity, enhanced rate of DNA synthesis and depletion of the antioxidant armoury of the tissue. In this study, we elucidate the effect of exogenous NO administration, using the NO donor glyceryl trinitrate (GTN), on KBrO3-induced nephrotoxicity, oxidative stress and cell proliferation. KBrO3 administration at a dose of 125 mg/kg body weight results in significant (P < 0.001) depletion in renal glutathione (GSH) content, and glutathione reductase (GR) activity with a concomitant increase in microsomal lipid peroxidation, and blood urea nitrogen (BUN) and creatinine levels. Parallel to these changes, we found significant enhancement in ornithine decarboxylase (ODC) activity and rate of renal DNA synthesis. Subsequent administration of GTN resulted in dose-dependent amelioration of GSH content and GR activity with concomitant inhibition of lipid peroxidation, and BUN and creatinine levels. In addition, GTN administration to KBrO3-intoxicated rats resulted in significant dose-dependent down regulation of enhanced ODC activity and rate of [3H]-thymidine incorporation in renal DNA, providing support for the protective role of NO in attenuation of KBrO3-induced oxidative stress and cell proliferation. Enhancement of oxidative tissue injury and cell proliferation on administration of the NO inhibitor, L-NAME, further demonstrates the protective efficacy of endogenous NO. These data suggest that NO inhibits KBrO3-induced tissue injury, oxidative stress and proliferative response in the rat kidney.
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PMID:Glyceryl trinitrate, a nitric oxide donor, suppresses renal oxidant damage caused by potassium bromate. 1077 65

We examined the role of the nitric oxide (NO) pathway on ischemia-reperfusion injury with the use of isolated perfused guinea pig hearts. We administered to the heart either L-arginine or N-nitro-L-arginine methyl ester (L-NAME) before or after 20 min of ischemia, and we observed the heart rate, aortic pressure, and contractile force, as well as the levels of malondialdehyde (MDA) and glutathione (GSH). We observed that L-NAME increased the tissue MDA levels and aortic pressure. On the other hand, L-arginine before the onset of reperfusion decreased aortic pressure and tissue MDA levels but increased the tissue GSH levels. We concluded that L-arginine administration before the onset of reperfusion improves myocardial recovery from ischemic injury.
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PMID:Role of the nitric oxide pathway on ischemia-reperfusion injury in an isolated perfused guinea pig heart. 1079 62

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


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