Literature DB >> 8198100

Decrease in ornithine decarboxylase activity after eradication of Helicobacter pylori.

K Alam1, F L Arlow, C K Ma, T T Schubert.   

Abstract

OBJECTIVE: Our aim was to determine whether gastric mucosal ODC activity is altered after successful eradication of HP. Recent reports have suggested that Helicobacter pylori (HP) infection of the stomach is associated with the development of gastric cancer. Gastrointestinal cancers usually do not arise de novo; a series of mucosal changes leading to neoplastic transformation and degrees of dysplasia are believed to precede the development of cancer. These conditions are associated with increased cellular proliferation. Ornithine decarboxylase (ODC) activity is induced by factors that stimulate cellular proliferation, and has been shown to be elevated in gastrointestinal neoplasia, including gastric cancer.
METHODS: Gastric antral and body biopsies were obtained from 17 HP-positive patients at endoscopy, for ODC activity and histology (including Warthin Starry stain) before and 4-6 wk after successful triple therapy.
RESULTS: Patients included 12 males and five females, with a mean age of 55 yr (27-73 yr). Mean ODC activity (in pmol CO2/mg protein/h) was significantly decreased after eradication of HP, compared with pretreatment levels in antral (147 +/- 26 vs. 80 +/- 15) and body mucosa (76 +/- 21 vs. 20 +/- 5) (p < 0.05).
CONCLUSION: Successful eradication of HP decreases mucosal proliferative activity, as reflected by decreased ODC activity. We speculate that by decreasing mucosal proliferative activity, HP eradication may help decrease the subsequent risk of gastric cancer.

Entities:  

Mesh:

Substances:

Year:  1994        PMID: 8198100

Source DB:  PubMed          Journal:  Am J Gastroenterol        ISSN: 0002-9270            Impact factor:   10.864


  7 in total

1.  Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases.

Authors:  J M Götz; J L Thio; H W Verspaget; G J Offerhaus; I Biemond; C B Lamers; R A Veenendaal
Journal:  Gut       Date:  1997-05       Impact factor: 23.059

Review 2.  Biochemical Features of Beneficial Microbes: Foundations for Therapeutic Microbiology.

Authors:  Melinda A Engevik; James Versalovic
Journal:  Microbiol Spectr       Date:  2017-10

3.  Gene expression of ornithine decarboxylase, cyclooxygenase-2, and gastrin in atrophic gastric mucosa infected with Helicobacter pylori before and after eradication therapy.

Authors:  Peter C Konturek; Kazimierz Rembiasz; Stanislaw J Konturek; Jerzy Stachura; Wladyslaw Bielanski; K Galuschka; Danuta Karcz; Eckhart G Hahn
Journal:  Dig Dis Sci       Date:  2003-01       Impact factor: 3.199

4.  L-arginine availability regulates inducible nitric oxide synthase-dependent host defense against Helicobacter pylori.

Authors:  Rupesh Chaturvedi; Mohammad Asim; Nuruddeen D Lewis; Holly M Scott Algood; Timothy L Cover; Preston Y Kim; Keith T Wilson
Journal:  Infect Immun       Date:  2007-06-11       Impact factor: 3.441

Review 5.  Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise.

Authors:  Alain P Gobert; Keith T Wilson
Journal:  Free Radic Biol Med       Date:  2016-09-25       Impact factor: 7.376

Review 6.  Bacterial infection as a cause of cancer.

Authors:  J Parsonnet
Journal:  Environ Health Perspect       Date:  1995-11       Impact factor: 9.031

7.  The Helicobacter pylori fatty acid cis-9,10-methyleneoctadecanoic acid stimulates protein kinase C and increases DNA synthesis of gastric HM02 cells.

Authors:  W Beil; B Obst; S Wagner; K F Sewing
Journal:  Br J Cancer       Date:  1998-06       Impact factor: 7.640

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.