NO Metabolites (no + metabolite)

Distribution by Scientific Domains

Selected Abstracts

Effect of garlic consumption on total antioxidant status and some biochemical and haematological parameters in blood of rats

Alireza Zamani
Abstract BACKGROUND: The effect of diet garlic supplementation on total antioxidant status (TAS), nitric oxide (NO) and routine biochemical and haematological parameters was investigated in blood of rats. A total of 30 male rats were divided equally into two groups. Each of 15 rats of treatment group was fed 600 mg kg,1 garlic solution in distilled water by gavage and controls only received distilled water. After garlic consumption for 1 month, blood serum total antioxidant, nitrate and some biochemical and haematological tests including serum lipids parameters, blood sugar, complete blood count (CBC), and haemoglobin were measured. RESULTS: The garlic treatment group showed significantly increase in the mean level of TAS from 0.77 ± 0.10 mol L,1 to 1.18 ± 0.11 mol L,1 (P < 0.01) and nitrate (a NO metabolite) from 0.78 ± 0.06 µmol L,1 to 1.44 ± 0.27 µmol L,1 (P < 0.05) in the blood sera of rats compared with the controls. There were no significant differences between the routine biochemical and haematological parameters. CONCLUSION: Garlic consumption should have antioxidant properties and may not affect the lipids profile and total blood cell counts. Copyright © 2009 Society of Chemical Industry [source]

Increased urinary excretion of nitric oxide metabolites in longitudinally monitored migraine patients

K. Rejdak
This study evaluated a relationship between nitric oxide (NO) and migraine attacks in order to gain insight into migraine pathomechanism. The study groups consisted of 12 migraineurs and eight controls. All subjects collected morning urine samples for 40 consecutive days. Urinary NO metabolites, nitrite/nitrate (NOx) levels were measured with the vanadium-based assay, whilst creatinine (Cr) and neopterin were determined with high-performance liquid chromatography. The mean urinary NOx/Cr ratio and number of NOx peaks was significantly greater in the migraine group compared with controls (P = 0.01 and P = 0.007, respectively). In the second approach, high NOx values were re-assessed in relation to raised neopterin, a marker of systemic infection or inflammation, and were excluded. The excretion of NOx persisted being pulsatile, and migraineurs had more peaks compared with controls (P = 0.01). In seven patients, NOx peaks coincided with headache days. This was more frequent than expected by random association in four patients (Monte-Carlo simulation; odds ratios: 2.16,7.77; no overlap of 95% CI). In four patients, NOx peaks preceded or followed headache days. Although there is a difference in the pattern of urinary NOx excretion between control and migraine populations, the variable temporal association of NOx peaks and headaches suggests a complex role of NO in this condition. [source]

Nitric Oxide Plays a Crucial Role in the Development/Progression of Nonalcoholic Steatohepatitis in the Choline-Deficient, l-Amino Acid-Defined Diet-Fed Rat Model

ALCOHOLISM, Issue 2010
Koji Fujita
Background:, The pathogenesis of nonalcoholic steatohepatitis (NASH) is still unclear. Recently, the 2-hit hypothesis was proposed, in which nitric oxide production, representing oxidative stress, was proposed as a very important candidate for the second hit. Methods:, The total study period was 10 weeks. A total of 20 rats were randomly divided into 2 groups. Group 1 was administered the Choline-Deficient, l-Amino Acid-Defined diet to produce a NASH model, and Group 2 as control received the Choline-Sufficient, l-Amino Acid-defined diet. The blood and tissue concentrations of nitrate + nitrite were measured using the Griess reagent and the expression levels of inducible nitric oxide synthase (iNOS) proteins and mRNA was determined by Western blotting. Results:, In regard to nitric oxide (NO) and NO metabolites, there were significant differences in the blood (especially portal venous blood) as well as tissue (liver and visceral fat) concentrations between the 2 animal groups; the amounts of NO metabolites in the tissues were much higher in the NASH models. The level of nitrotyrosine was much markedly higher in the NASH models than in the controls. In regard to the tissue expression of iNOS a significant difference between the 2 groups was found in the visceral fat, especially in the mesenterium. Conclusions:, Based on these results, we hypothesize that the iNOS expression and NO levels in the visceral fat increase, with increased diffusion of NO and its metabolites into the liver, resulting in increased nitrotyrosine formation in the liver; this, in turn, induces inflammation, apoptosis, and fibrosis in the liver, which are one of the characteristic features of NASH. [source]

Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs

K. Takeuchi
Summary Background: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). Aim: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. Methods: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 m m taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or NG -nitro- l -arginine methyl ester (L-NAME). Results: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. Conclusions: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine. [source]

Spontaneous labor increases nitric oxide synthesis during the early neonatal period

Akihiko Endo
AbstractBackground: This paper aimed to assess the influence of spontaneous labor upon endogenous nitric oxide (NO) and endothelin 1 (ET-1) during transition to extrauterine life. Methods: The serum levels of NO metabolites (the sum of nitrites and nitrates (NOx)) and the plasma level of ET-1 were determined in 53 healthy full-term infants (spontaneous labor group; n=40, cesarean delivery group; n=13). In both groups, blood samples were obtained from a cord vein at birth and from a peripheral vein at 5 days of age. Results: The differences in serum NOx concentrations between the spontaneous labor group and the elective cesarean group were not significant at birth. By the age of 5 days, serum NOx concentrations had risen significantly in the spontaneous labor group to become significantly higher in the elective cesarean group. Conclusion: It is speculated that spontaneous labor might enhance endogenous NO synthesis at 5 days of age. [source]

Vasoactive factors in sickle cell disease: In vitro evidence for endothelin-1-mediated vasoconstriction

Sitki Ergul
Abstract While systemic plasma endothelin-1 (ET-1) levels are increased during acute crisis in sickle cell disease, the relative levels of potent vasoactive factors that contribute to the regulation of vascular function, such as ET-1, NO, and cell-free hemoglobin, during the course of periodic vaso-occlusive episodes remain unclear. Moreover, whether and to what extent sickling-induced release of ET-1 alters vascular tone is not completely understood. To investigate the sequential changes in circulating vasoactive factors, we measured plasma ET-1, NO metabolites (NOx), and cell-free hemoglobin (Hb) before (steady-state), during (crisis), and after a vaso-occlusive (post-crisis) episode. Steady-state ET-1 levels (fmol/mL) increased from 2.3 ± 0.4 to 11.0 ± 1.4 and 4.2 ± 1.0 during crisis and post-crisis periods, respectively. There was no significant difference in plasma NOx levels. Cell-free Hb levels were significantly higher in sickle cell patients in all phases as compared to the control group, and especially during crisis cell-free Hb levels were elevated by 4-fold (209,000 ± 31,000 vs. 46,000 ± 5,300 ng/mL in steady-state). Conditioned medium from human pulmonary artery endothelial cells exposed to sickled erythrocytes prepared by deoxygenation induced contraction of aortic rings, and this effect was blocked by an ETA receptor antagonist. These findings indicate that ET-1 is the predominant contractile factor released by cultured endothelial cells upon exposure to deoxygenated sickled SS erythrocytes and ET-1,NO,NO scavenger balance is altered in favor of vasoconstriction during an acute episode in SCD. Am. J. Hematol. 76:245,251, 2004. © 2004 Wiley-Liss, Inc. [source]

Preservation of Endothelium Nitric Oxide Release by Pulsatile Flow Cardiopulmonary Bypass When Compared With Continuous Flow

Ettore Lanzarone
Abstract The aim of this work is to analyze endothelium nitric oxide (NO) release in patients undergoing continuous or pulsatile flow cardiopulmonary bypass (CPB). Nine patients operated under continuous flow CPB, and nine patients on pulsatile flow CPB were enrolled. Plasma samples were withdrawn for the chemiluminescence detection of nitrite and nitrate. Moreover the cellular component was withdrawn for the detection of nitric oxide synthase (NOS) activity in the erythrocytes, and an estimation of systemic inflammatory response was carried out. Significant reduction in the intraoperative concentration with respect to the preoperative was observed only under continuous flow CPB for both nitrite and NOx (nitrite + nitrate) concentration (P = 0.010 and P = 0.016, respectively). Significant difference in intraoperative nitrite concentration was also observed between the groups (P = 0.012). Finally, erythrocytes showed a certain endothelial NOS activity, which did not differ between the groups, and no differences in the inflammatory response were pointed out. The significant reduction of NO2 - concentration under continuous perfusion revealed the strong connection among perfusion modality, endothelial NO release, and plasmatic nitrite concentration. The similar erythrocyte eNOS activity between the groups revealed that the differences in blood NO metabolites are mainly ascribable to the endothelium release. [source]

Attenuation of reperfusion injury by renal ischaemic preconditioning: the role of nitric oxide

M.K. Jefayri
Objective To determine the effect on nitric oxide (NO) release and renal NO synthase (endothelial, eNOS and inducible, iNOS) activity of renal ischaemia-reperfusion (I/R) in vivo in an animal model, and to examine the possible involvement of NO in ischaemic preconditioning (IP) of the kidney. Materials and methods In a right-nephrectomized rat model, 42 animals were randomized in four groups: controls; IP-only (4 min of ischaemia followed by 11 min of reperfusion, total of four cycles); renal warm ischaemia (45 min) and 6 h reperfusion; ischaemia (45 min) preceded by IP pretreatment. Serum NO metabolites were assayed 2 and 6 h after ischaemia or the control equivalent. NOS expression in the kidney was detected immuno-histochemically, and damage assessed morphologically in sections stained with haematoxylin and eosin. Kidney function was assessed by the levels of serum creatinine, urea and electrolytes. Results Compared with before ischaemia, the concentration of serum NO metabolites at 6 h was increased in the IP-only animals (P = 0.016) and in the IP + I/R group (P = 0.002). There was greater eNOS expression in the IP-only group (P = 0.009) and in the IP + I/R group than in controls (P = 0.050). iNOS expression was greater in the IP-only animals than in the control group (P = 0.050). Histological assessment showed less evidence of cellular damage in IP + I/R animals than in the I/R-alone group (P = 0.020). Serum creatinine level was not significantly different between the IP-only group and the control. There were no differences after 2 h of reperfusion. Conclusion Ischaemic preconditioning has a protective effect on renal structure and function, which may be produced by increased NO release arising from increased NOS expression by 6 h after reperfusion. [source]

Nitrite, NO and hypoxic vasodilation

Jason D Allen
The ability to deliver oxygen and other nutrients to working tissues at a rate acutely matched to demand is the quintessential function of the cardiovascular system. Thus, an understanding of the biochemical mechanisms involved in hypoxic vasodilation remains a major goal in vascular biology. Nitric oxide, its metabolites, and oxidation status are recognized as playing important roles in this process. Previous work examining how nitrite can be converted to bioactive nitric oxide (NO) under hypoxic conditions has focused on the role of the red blood cell and haemoglobin. In a recent issue of the British Journal of Pharmacology, Pinder et al. demonstrate that plasma nitrite, in the absence of haemoglobin, is capable of increasing the maximal dilation of rabbit aortic rings under hypoxic conditions. Furthermore, they demonstrate that this relaxation can occur with or without the endothelium. This observation, even if it is only a small proportion of the relaxant activity of nitrite, highlights how NO metabolites may be involved in a variety of mechanisms of vessel control. [source]

Differential regulation of nitric oxide synthase isoforms in experimental acute Chagasic cardiomyopathy

B. Chandrasekar
We have previously demonstrated induction and high level expression of IL-1,, IL-6 and tumour necrosis factor-alpha in the myocardium during the acute stage of experimental Trypanosoma cruzi infection (Chagas' disease). The myocardial depressive effects of these cytokines are mediated in part by the induction of nitric oxide synthase (NOS), production of nitric oxide (NO) and formation of peroxynitrite. In this study we investigated the expression, activity and localization of NOS isoforms, and the levels of NO, malondialdehyde (a measure of oxidative stress), and peroxynitrite in rats at 1·5, 5, 10 and 15 days after infection with T. cruzi trypomastigotes. The myocardial inflammatory infiltrate and number of amastigote nests increased over the course of infection. A significant increase in tissue nitrate + nitrite levels, NOS2 mRNA, and NOS2 enzyme activity was observed at all time points in the infected compared with uninfected animals. The enzyme activity of constitutive NOS, tissue malondialdehyde levels, and NOS3 mRNA levels was only transiently increased after infection. The protein levels of the NOS isoforms paralleled their mRNA expression. While no positive nitrotyrosine immunoreactivity was detected in control myocardium, its levels increased in infected animals over time. Thus, by 1·5 days post-infection, when no parasite or immune cell infiltration could be detected, the myocardium expressed high levels of NOS and NO metabolites. Nevertheless, the early production of NO in the myocardium was not sufficient to clear the parasites. [source]


Kazushi Tsuda
SUMMARY 1The purpose of the present study was to assess the possible link between plasma homocysteine and membrane fluidity in normotensive and hypertensive men. 2The membrane fluidity (a reciprocal value of membrane microviscosity) of red blood cells (RBC) was measured using an electron paramagnetic resonance and spin-labelling method. The membrane fluidity of RBC was decreased in hypertensive compared with normotensive men. 3Total plasma homocysteine levels were significantly higher in hypertensive men than normotensive men. In contrast, plasma levels of nitric oxide (NO) metabolites were significantly lower in hypertensive men than in normotensive men. The decreased membrane fluidity of RBC was associated with hyperhomocysteinaemia and reduced plasma levels of NO metabolites. 4The results of the present study suggest that hyperhomocysteinaemia may have a role in modulating the rheological behaviour of RBC and microcirculation in men by, at least in part, reducing NO bioavailability. [source]

Cerebral Thrombosis And Microcirculation Of The Rat During The Oestrous Cycle And After Ovariectomy

H Ono
SUMMARY 1. The effects of oestrogen on thrombogenesis and the cerebral microcirculation of the female rat were studied during the oestrous cycle and after ovariectomy. 2. Serum levels of oestradiol (E2) and plasma concentrations of nitric oxide (NO) metabolites were significantly greater at pro-oestrus than at dioestrus. Blood vessel diameter, mean red cell velocity, wall shear rate and blood flow at pro-oestrus were significantly higher than at dioestrus. Thrombotic tendency, assessed using a He,Ne laser-induced thrombosis model, was significantly decreased at pro-oestrus compared with dioestrus. 3. The long-term deprivation of oestrogen by ovariectomy significantly depressed serum levels of E2 and plasma concentrations of NO metabolites. Thrombotic tendency was significantly increased 4 weeks after ovariectomy. Vessel diameter, mean red cell velocity, wall shear rate and blood flow in pial arterioles were significantly reduced after ovariectomy. 4. Exogenous administration of oestrogen (17,-oestradiol) after surgery reversed the increased thrombotic tendency mediated by ovariectomy. 5. These results strongly indicate that oestrogen mediates beneficial effects on the cerebral microcirculation and moderates cerebral thrombotic mechanisms in the female rat. [source]