A Novel Nonenzymatic Pathway for the Generation of Nitric Oxide by the Reaction of Hydrogen Peroxide and D- or L-Arginine

Nagase, Sohji; Takemura, Katsumi; Ueda, Atsushi; Hirayama, Aki; Aoyagi, Kazumasa; Kondoh, Motohiro; Kôyama, Akio

doi:10.1006/bbrc.1997.6428

Cited by 161 publications

(99 citation statements)

References 15 publications

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“…However, the present findings do not provide information on a putative NO overproduction in the jejunal wall induced by chronic alcohol consumption, or on whether this NO is generated by iNOS expressed in myenteric neurons (Valentine et al, 1996;Mulè et al, 2001;Vannucchi et al, 2002), enteric glial cells (Green et al, 2004), or by NOSindependent NO-producing mechanisms in the GI tract (Goretski et al, 1990;Nagase et al, 1997).…”

Section: Discussionmentioning

confidence: 67%

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

Bagyánszki

Krecsmarik

Winter

et al. 2010

The Anatomical Record

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Alcohol consumption interferes with gastrointestinal transit causing symptoms in alcoholic patients. Nitric oxide (NO), synthesized by neuronal nitric oxide synthase (nNOS) plays an important role in the control of gastrointestinal motility. Our aim was to investigate whether chronic alcohol intake in a murine model induces gastrointestinal motility disturbances and affects the nitrergic myenteric neurons in the stomach and jejunum. Gastric emptying, small intestinal transit and geometric centre were measured in vivo after intragastric gavage of Evans blue. Nitrergic relaxations to electrical field stimulation (EFS) and exogenous NO were recorded in jejunal muscle strips in vitro. The proportion of nNOS-immunopositive myenteric neurons was assessed using PGP9.5 and nNOS immunostaining. After chronic alcohol consumption, gastric emptying and small intestinal transit were delayed compared with control mice, and the nitrergic nervemediated relaxations to EFS in the jejunum were decreased, whereas relaxations to exogenous NO did not differ. The proportion of nNOS-immunoreactive neurons did not change in the stomach, whereas in the jejunum the percentage decreased from 33% to 27% (P < 0.001) after chronic alcohol intake. The total number of myenteric neurons remained unchanged. These results suggest that chronic alcohol consumption disturbs gastric and small intestinal motility in vivo and in vitro and is associated with a decrease in the proportion of nNOS-immunoreactive myenteric neurons in the murine jejunum. Anat Rec, 293:1536Rec, 293: -1542Rec, 293: , 2010.

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Section: Discussionmentioning

confidence: 67%

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

Bagyánszki

Krecsmarik

Winter

et al. 2010

The Anatomical Record

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“…To further prove that the observed NO-heme complex formation was derived from nitrite, isotope tracer experiments were performed measuring nitrosyl-heme formation in hearts infused with isotopically labeled [ 15 (Fig 6B), whereas with [ 14 N]nitrite the typical 14 NO-Mb spectrum was observed (Fig. 6A).…”

Section: Resultsmentioning

confidence: 99%

“…Also, increasing levels of nitrite resulted in increased complex formation. Furthermore, isotope tracer studies using 15 N-labeled nitrite demonstrated that the NO was derived from nitrite. Thus, tissue nitrite levels are of critical importance in this process.…”

Section: Discussionmentioning

confidence: 99%

“…These are dependent on the reduction or disproportionation of the substrate nitrite, and with increasing periods of ischemia, where there is increasingly severe hypoxia and acidosis, these NOS-independent pathways become the major source of tissue NO production (10,12,13) There are several reaction mechanisms that have been shown to lead to NOS-independent NO production. These include acidotic degradation of tissue nitrite to NO (10,14) and reaction between arginine and H 2 O 2 to form NO (15) as well as the reduction of nitrite to NO catalyzed by microbial nitrite reductase (16). Recently, it has been reported that xanthine oxidoreductase-catalyzed reduction of nitrite to NO also occurs under hypoxic conditions (17)(18)(19)(20).…”

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confidence: 99%

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Nitrosyl-Heme Complexes Are Formed in the Ischemic Heart

Tiravanti

Samouilov

Zweíer

2004

Journal of Biological Chemistry

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In addition to the generation from specific nitric-oxide (NO) synthases, NO formation from nitrite occurs in ischemic tissues, such as the heart. Although NO binding to heme-centers is the basis for NO-mediated signaling as occurs through guanylate cyclase, it is not known if this process is triggered with physiologically relevant periods of sublethal ischemia and if nitrite serves as a critical substrate. Therefore electron paramagnetic resonance studies were performed to measure nitrosylheme formation during the time course of myocardial ischemia and reperfusion and the role of nitrite in this process. Rat hearts were either partially nitrite-depleted by nitrite-free buffer perfusion or nitrite-enriched by preinfusion with 50 M nitrite. Ischemic hearts loaded with nitrite showed prominent spectra of six-coordinate nitrosyl-heme complexes, primarily NOmyoglobin, that increased as a function of ischemic duration, whereas in nonischemic-controls these signals were not seen. Total nitrosyl-heme concentrations within the heart were 6.6 ؎ 0.7 M after 30 min of ischemia. Nitrite-depleted hearts also gave rise to NO-heme signals during ischemia, but levels were 8-fold lower. Nitrite-mediated NO-heme complex formation during ischemia was associated with activation of guanylate cyclase. Upon reperfusion, the levels of NO-heme complexes decreased 3-fold by the first 15 min but remained elevated for over 45 min. The decrease in NO-heme complex levels was paralleled by the formation of nitrate, suggesting the oxidation of heme-bound NO upon reperfusion. Thus, nitrite-mediated NO-heme formation occurs progressively during ischemia, with these complexes serving as a store of NO with concordant activation of NO signaling pathways.

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“…These routes include spontaneous reduction of tissue nitrite to NO under acidotic conditions, e.g. in the ischaemic heart [87,88], and reaction between L-or D-arginine and some arginine derivatives with hydrogen peroxide to form NO [89,90]. There are other "non-enzymatic" sources which may contribute to the local levels of NO, although in less extent and some times in conquer to the enzymatic production.…”

Section: 13mentioning

confidence: 99%

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

Boudko

2007

Journal of Chromatography B

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This review briefly summarizes recent progress in fundamental understanding and analytical profiling of the L-arginine/nitric oxide (NO) pathway. It focuses on key analytical references of NO actions and on the experimental acquisition of these references in vivo, with capillary electrophoresis (CE) and high-performance capillary electrophoresis (HPCE) comprising one of the most flexible and technologically promising analytical platform for comprehensive high-resolution profiling of NO-related metabolites. Second aim of this review is to express demands and bridge efforts of experimental biologists, medical professionals and chemical analysis-oriented scientists who strive to understand evolution and physiological roles of NO and to develop analytical methods for use in biology and medicine.

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A Novel Nonenzymatic Pathway for the Generation of Nitric Oxide by the Reaction of Hydrogen Peroxide and D- or L-Arginine

Cited by 161 publications

References 15 publications

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

Chronic Alcohol Consumption Affects Gastrointestinal Motility and Reduces the Proportion of Neuronal NOS‐Immunoreactive Myenteric Neurons in the Murine Jejunum

Nitrosyl-Heme Complexes Are Formed in the Ischemic Heart

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

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