Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage

Murakami, Motonobu; Asagoe, Kohsuke; Dekigai, Hiroshi; Kusaka, Satoshi; Saita, Hiroshi; Kita, Toru

doi:10.1007/bf02065408

Cited by 64 publications

(46 citation statements)

References 26 publications

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“…1, 4) Suzuki et al [65] and Murakami et al [66] have reported that H. pylori increases the production of inflammatory cytokines such as IL-1b, IL-2, IL-6, IL-8, and tumor necrosis factor alpha (TNF-a), and that toxic metabolites and lysosomal enzymes released from neutrophils are also responsible for gastric mucosal injury, while Takashima et al [67] reported that decreased acid secretion was accompanied by an elevation of IL-1b messenger RNA levels in the H. pylori-infected gastric mucosa. Esplugues et al [68] and Kondo et al [69] reported that the acidinhibitory effect of IL-1b appears to involve nitric oxide synthesis and may be mediated by the inhibition of gastric histamine mobilization.…”

Section: Endogenous Factorsmentioning

confidence: 96%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

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Section: Endogenous Factorsmentioning

confidence: 96%

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

et al. 2011

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“…The resultant HClO, in turn, interacts with ammonia to generate monochloramine (NH 2 Cl), a high toxic substance on gastric mucosa (2,3). Several studies have reported that either exogenous or endogenous NH 2 Cl at much lower concentrations than ammonia produces gastric mucosal lesions in rats (4,5).…”

Section: Introductionmentioning

confidence: 99%

Irsogladine Prevents Monochloramine-Induced Gastric Mucosal Lesions by Improving the Decrease in Mucosal Blood Flow Due to the Disturbance of Nitric Oxide Synthesis in Rats

et al. 2003

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Abstract. The inhibitory effect of an anti-ulcer drug irsogladine [2,4-diamino-6-(2,5-dichlorophenyl)-s-triazine maleate] on monochloramine (NH 2 Cl)-induced gastric mucosal lesions and its mechanisms of action were clarified in rats. Irsogladine dose-dependently prevented the formation of gastric mucosal lesions induced by 60 mM NH 2 Cl. The mucosal protective effect of irsogladine was not influenced by capsaicin-sensitive sensory defunctionalization. On the other hand, its protective effect was diminished by the inhibitor of nitric oxide synthase N G -nitro-Larginine methylester (L-NAME), but not by the inducible nitric oxide synthase selective inhibitor aminoguanidine. Irsogladine restored the NH 2 Cl-induced decrease in the gastric cGMP formation as an index of nitric oxide synthesis, while it alone had no influence on the cGMP formation in intact tissues. Pretreatment with L-NAME abolished the recovery of cGMP by irsogladine. Furthermore, irsogladine ameliorated the NH 2 Cl-induced decrease in gastric mucosal blood flow, which was also reversed by pretreatment with L-NAME. These findings suggest that the improvement of the decrease in mucosal blood flow subsequent to the disturbance of gastric nitric oxide synthesis is involved in the protective effect of irsogladine on gastric mucosal lesions caused by NH 2 Cl.

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“…5,6 Thus, it is possible that NH 4 OH, even at low concentrations, produces NH 2 Cl by interaction with HClO in the ischaemic stomach, resulting in damage to the gastric mucosa. Indeed, Murakami et al 9 have previously reported that the gastric irritable effect of low concentrations of NH 4 OH under ischaemia is totally abolished by antineutrophil serum. Moreover, we observed that exogenously administered NH 2 Cl, a mixture of NH 4 OH and NaHClO, which at low concentrations does not produce any damage to the mucosa, caused severe haemorrhagic lesions in the gastric mucosa of unanaesthetized rats.…”

Section: Discussionmentioning

confidence: 97%

“…7,8 Indeed, it has been demonstrated that NH 2 Cl plays a role in the pathogenesis of NH 4 OHinduced gastric lesions in rats. 9,10 We have also reported that both endogenous and exogenous NH 2 Cl damage the gastric mucosa at much lower concentrations than NH 4 OH. 11,12 In addition, we have recently SUMMARY Background: It is well known that neutrophil-derived hypochlorous acid interacts with ammonia (NH 4 OH) to generate monochloramine (NH 2 Cl) and that NH 2 Cl irritates the gastric mucosa and impairs ulcer healing.…”

Section: Introductionmentioning

confidence: 93%

Effect of taurine on ulcerogenic response and impaired ulcer healing induced by monochloramine in rat stomachs

Kato

Umeda

Takeeda

et al. 2002

Aliment Pharmacol Ther

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INTRODUCTIONHelicobacter pylori has been recognized as the major cause of gastritis and peptic ulcer diseases. [1][2][3] This bacterium has high urease enzyme activity, resulting in an abnormally high concentration of ammonia (NH 4 OH) in the stomach of infected patients. 3 Given that H. pylori-associated chronic active gastritis is characterized by the invasion of neutrophils into the gastric mucosa 1, 3, 4 and that neutrophils utilize the H 2 O 2 -myeloperoxidase-halide system to generate an oxidant capable of destroying a variety of mammalian cell targets as well as micro-organisms, 5,6 it is assumed that neutrophil-derived hypochlorous acid (HClO) interacts with NH 4 OH to generate cytotoxic monochloramine (NH 2 Cl). 7,8 Indeed, it has been demonstrated that NH 2 Cl plays a role in the pathogenesis of NH 4 OHinduced gastric lesions in rats. 9, 10 We have also reported that both endogenous and exogenous NH 2 Cl damage the gastric mucosa at much lower concentrations than NH 4 OH. 11,12 In addition, we have recently SUMMARY Background: It is well known that neutrophil-derived hypochlorous acid interacts with ammonia (NH 4 OH) to generate monochloramine (NH 2 Cl) and that NH 2 Cl irritates the gastric mucosa and impairs ulcer healing. Aim: To examine the effect of taurine, a hypochlorous acid scavenger, on the mucosal ulcerogenic and the impaired healing response induced by NH 2 Cl in rat stomachs, in comparison with those of methionine and glycine. Methods and results: Under anaesthesia, oral administration of NH 2 Cl (120 mmol/L) produced severe lesions in male Sprague-Dawley rat stomachs. Taurine (10-100 mg/kg) given p.o. 30 min prior to NH 2 Cl dosedependently prevented these lesions in response to NH 2 Cl. This action was mimicked by methionine (3-30 mg/kg) but not by glycine (10-100 mg/kg). Under urethane anaesthesia, mucosal exposure to NH 4 OH (120 mmol/L) caused a marked reduction of potential difference (PD) in the ex vivo chambered stomachs after

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Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage

Cited by 64 publications

References 26 publications

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

Irsogladine Prevents Monochloramine-Induced Gastric Mucosal Lesions by Improving the Decrease in Mucosal Blood Flow Due to the Disturbance of Nitric Oxide Synthesis in Rats

Effect of taurine on ulcerogenic response and impaired ulcer healing induced by monochloramine in rat stomachs

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