Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations.

Sobala, G. M.; Schorah, C. J.; Shires, S E; Lynch, D. A. F.; Gallacher, Beverley; Dixon, M. F.; Axon, Anthony

doi:10.1136/gut.34.8.1038

Cited by 144 publications

(90 citation statements)

References 10 publications

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“…While activated, ROSreleasing phagocytic leukocytes recruited to the gastric mucosa during infection represent one obvious source of oxidative stress (21,79), other studies demonstrate that H. pylori itself also generates ROS (51) and that ROS accumulate in gastric epithelial cells (5,6,73). In addition, proinflammatory cytokines induce ROS in various cell types (47,48,61), and the decreased levels of ascorbic acid that are associated with H. pylori infection (64,71) also contribute to a pro-oxidative environment. H. pylori infection has been shown to increase expression and activity of spermine oxidase, which oxidizes polyamines that are abundant in epithelial cells to release hydrogen peroxide (77), suggesting another mechanism by which H. pylori induces oxidative stress.…”

mentioning

confidence: 99%

Helicobacter pyloriInfection Induces Oxidative Stress and Programmed Cell Death in Human Gastric Epithelial Cells

Ding¹,

Minohara²,

Fan³

et al. 2007

Infect Immun

178

137

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Helicobacter pylori infection is associated with altered gastric epithelial cell turnover. To evaluate the role of oxidative stress in cell death, gastric epithelial cells were exposed to various strains of H. pylori, inflammatory cytokines, and hydrogen peroxide in the absence or presence of antioxidant agents. Increased intracellular reactive oxygen species (ROS) were detected using a redox-sensitive fluorescent dye, a cytochrome c reduction assay, and measurements of glutathione. Apoptosis was evaluated by detecting DNA fragmentation and caspase activation. Infection with H. pylori or exposure of epithelial cells to hydrogen peroxide resulted in apoptosis and a dose-dependent increase in ROS generation that was enhanced by pretreatment with inflammatory cytokines. Basal levels of ROS were greater in epithelial cells isolated from gastric mucosal biopsy specimens from H. pylori-infected subjects than in cells from uninfected individuals. H. pylori strains bearing the cag pathogenicity island (PAI) induced higher levels of intracellular oxygen metabolites than isogenic cag PAI-deficient mutants. H. pylori infection and hydrogen peroxide exposure resulted in similar patterns of caspase 3 and 8 activation. Antioxidants inhibited both ROS generation and DNA fragmentation by H. pylori. These results indicate that bacterial factors and the host inflammatory response confer oxidative stress to the gastric epithelium during H. pylori infection that may lead to apoptosis.Helicobacter pylori infection has been implicated in the pathogenesis of gastritis, peptic ulcer disease, gastric carcinoma, and gastric lymphoma (10, 18), but the mechanisms leading from chronic active gastritis to other disease manifestations remain unclear. Various bacterial factors as well as the host response are believed to contribute to the outcome of infection with H. pylori (25). Strains bearing the cag pathogenicity island (PAI) (15), which includes the cagA gene, have been shown to be associated with increased gastric inflammation (57), increased bacterial load, and both peptic ulcer disease and gastric cancer (11). Increased induction of gastric epithelial cytokines that recruit and activate immune/inflammatory cells is also observed with these strains (17,41,55,67). Although the full functions of genes included in the cag PAI remain unclear, it is known that cag PAI-positive strains activate specific transcription factors and cell signaling pathways (37,41,52,55,66).Bacterial and host factors can damage the gastric mucosal barrier and lead to alterations of epithelial cell growth and differentiation. H. pylori infection is associated with increased cellular proliferation in vivo (13, 43) although most in vitro studies demonstrate bacterial inhibition of cell growth (76), suggesting that factors other than H. pylori regulate cell growth in the complex milieu of the infected gastric mucosa. Increased numbers of apoptotic cells are found in the gastric epithelium of infected patients (36,45,50,58), suggesting that induction of apoptosis may b...

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mentioning

confidence: 99%

Helicobacter pyloriInfection Induces Oxidative Stress and Programmed Cell Death in Human Gastric Epithelial Cells

Ding¹,

Minohara²,

Fan³

et al. 2007

Infect Immun

178

137

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“…H. pylon-induced inflammation may facilitate gastric carcinogenesis by increasing the rate of cell replication. decreasing the concentration of ascorbic acid and inducing DNA damage via reactive oxygen species (Sobala et al 1993: Bechi et al 1996. It is worth noting that the prevalence of IM is also closely related to H. pylon infection (Rugge et al 1996).…”

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confidence: 99%

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

Shun²,

Lee³

et al. 1998

Br J Cancer

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(Correa. 1992). In sequential changes from superficial gastritis to dysplasia and cancer. intestinal metaplasia (TM) plays a pivotal role. This is testified by a high frequency of IM in patients with GC and in their relatives. a similar topographic distribution of IM and GC. and a high IM occurrence in endemic areas with a high risk of GC (Dobrilla et al. 1994). Although most investigators agree with Stemmermann ( 1994) that the risk of GC is proportional to the extent of IM and although IM has been intensively explored as a possible premalignant lesion of GC. controversy exists because of many confounding factors in previous retrospective studies (Antonioli. 1994). Because of the heterogeneous nature of IM. a recent interest has been focused on the interrelationship between GC and different subtypes of IM (Jass et al. 1979: Turani et al. 1986: Filipe et al. 1994 patients were finally included in this study. Tumorous. adjacent and non-tumorous portions were resected from surgical specimens and stored for further examination. Controls matched one-to-one with cases on age (within 3 years). sex. ethnic group and residential area were also selected from subjects receiving endoscopic examinations that did not reveal any ulcer nor tumour in the stomach. During this procedure. five specimens were biopsied including two from the lesser curvature of the antrum. one from the incisura angularis and two from the lesser curvature of the corpus of the stomach. An aliquot of 5 ml of heparinized blood wvas collected from each study subject. and the serum was separated on the same day and stored at -70°C until further testing. The titre of serum IgG antibody against H. pylorn was determined using an enzyme-linked immunosorbent assay as previously described (Lin et al. 1993).Histopathological determination of intestinal metaplasia and its subtypes Specimens from patients and controls were fixed in 10% buffered formalin. embedded in paraffin. sectioned and stained with haematoxylin and eosin (H&E). If IM was present in H&E staining, a fther section was stained using the high iron diamine (HID)alcian Table 2. There were 57 patients with diffuse type GC and 78 with intestinal type GC. According to the depth of invasion. the frequency of early lesion in diffuse type GC (42 .1%) was higher than that of intestinal type GC (29.5%7. P = 0.18).Intestinal type GC had a significantly higher frequency of coexistent IM (91.0%) than diffuse type (33.3%. P = 0.0001).As shown in Table 3

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“…It was found that the eradication of Helicobacter pylori by metronidazole improves secretion of vitamin C (an antioxidant) into the gastric juice, which may lead to an increased protection against gastric cancer. 38 In addition, there has been luminal release of epidermal growth factor into the stomach in healthy subjects and in duodenal ulcer patients following triple therapy, which plays a crucial role in the duodenal ulcer healing process. 20 Furthermore, combined treatment with metronidazole has also shown a protection against platelet Ó 1997 Blackwell Science Ltd, Aliment Pharmacol Ther 11, 811±819 activating factor-induced shock and the resulting intestinal necrosis.…”

Section: Discussionmentioning

confidence: 99%

The vascular and glandular organoprotective properties of metronidazole in the rodent stomach

Ching

Chow

et al. 1997

Aliment Pharmacol Ther

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INTRODUCTIONHelicobacter pylori is known to play a signi®cant aetiopathogenetic role in peptic ulcer disease. Triple therapy using colloidal bismuth subcitrate in combination with amoxycillin and metronidazole has been shown not only to heal peptic ulcers but also to prevent their recurrence. 1, 2 In a previous study, we demonstrated that amoxycillin, in addition to its antimicrobial action, imparted gastric cytoprotection through the action of prostaglandins in the gastric mucosa. 3 The present study aimed to determine whether metronidazole, one of the most commonly used antimicrobials for anti-Helicobacter pylori therapy, has similar organoprotective properties. In order to test this hypothesis, both ethanol and indomethacin ulcer models were employed in the rats. Evaluation of gastric mucosal mucus, prostaglandin E 2 (PGE 2 ) content, blood¯ow and potential difference across the mucosa were performed because these parameters have been shown to be the key factors in the maintenance of gastric mucosal integrity. 4±8 Furthermore, the effects of metronidazole on the vascular and glandular integrity of the stomachs of SUMMARY Background: The gastroprotective action of metronidazole, an antimicrobial used in the therapy against Helicobacter pylori infection, is unclear. Thus, the aim of the present investigation was to study the organoprotective action and antiulcer mechanisms of this drug in rodents. Methods and results: Metronidazole (10 mg/kg), given either per os or intraperitoneally, 30 min beforehand, reduced ethanol (40%, 10 mL/kg, p.o.)-induced gastric mucosal damage in male rats. Likewise, oral administration of metronidazole dose-dependently attenuated the indomethacin (30 mg/kg, p.o.)-induced gastric lesion formation and the concurrent depletion of mucosal mucus. However, metronidazole did not affect the basal mucosal prostaglandin E 2 content. In an ex vivo gastric chamber preparation, 40% ethanol incubation markedly lowered transmucosal potential

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Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations.

Cited by 144 publications

References 10 publications

Helicobacter pyloriInfection Induces Oxidative Stress and Programmed Cell Death in Human Gastric Epithelial Cells

Helicobacter pyloriInfection Induces Oxidative Stress and Programmed Cell Death in Human Gastric Epithelial Cells

Gastric cancer risk in relation to Helicobacter pylori infection and subtypes of intestinal metaplasia

The vascular and glandular organoprotective properties of metronidazole in the rodent stomach

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