Abstract

Background: Liver cirrhosis is associated with intestinal epithelial barrier dysfunction, which may be affected by oxidative stress. Studies in cirrhotic rats provided evidence for intestinal oxidative stress, but studies in cirrhotic patients are scarce. We have shown intestinal barrier dysfunction in patients with compensated cirrhosis. AIM: The present study aimed to investigate whether oxidative stress occurs in the intestinal mucosa of compensated cirrhotic patients and may contribute to barrier dysfunction. Material and methods: Oxidative stress was studied in duodenal and sigmoid biopsies from 15 cirrhotic patients and 22 controls by analyzing transcription of genes involved in glutathione and uric acid metabolism using quantitative real-time polymerase chain reaction. Protein levels of glutathione and glutathione disulphide were measured and the glutathione/glutathione disulphide ratio was calculated as marker of oxidative stress. In addition, intestinal myeloperoxidase and fecal calprotectin were determined. Result: Gene transcription of glutathione synthetase and glutathione reductase were significantly different in duodenal and sigmoid biopsies of cirrhotic patients vs. controls, but no alterations were found for other genes nor for glutathione, glutathione disulphide, glutathione/glutathione disulphide ratio and intestinal myeloperoxidase and fecal calprotectin concentrations. Conclusion: This study did not find indications for oxidative stress and low-grade inflammation in the small and large intestine of stable compensated cirrhotic patients. Although these preliminary findings need further validation, we found intestinal oxidative stress not to be a major mechanism contributing to epithelial barrier dysfunction in patients with compensated cirrhosis.

Original languageEnglish
Pages (from-to)402-409
Number of pages8
JournalAnnals of Hepatology
Volume15
Issue number3
DOIs
Publication statusPublished - 2016

Keywords

  • Intestine
  • Epithelial barrier
  • Glutathione
  • Inflammation
  • BACTERIAL TRANSLOCATION
  • BARRIER DYSFUNCTION
  • MUCOSAL ALTERATIONS
  • NITRIC-OXIDE
  • PERMEABILITY
  • INFLAMMATION
  • RATS
  • COMPLICATIONS
  • ANTIOXIDANTS
  • DISRUPTION

Cite this

@article{56a9246345624c46a0d5dbf649053d3e,
title = "Is intestinal oxidative stress involved in patients with compensated liver cirrhosis?",
abstract = "Background: Liver cirrhosis is associated with intestinal epithelial barrier dysfunction, which may be affected by oxidative stress. Studies in cirrhotic rats provided evidence for intestinal oxidative stress, but studies in cirrhotic patients are scarce. We have shown intestinal barrier dysfunction in patients with compensated cirrhosis. AIM: The present study aimed to investigate whether oxidative stress occurs in the intestinal mucosa of compensated cirrhotic patients and may contribute to barrier dysfunction. Material and methods: Oxidative stress was studied in duodenal and sigmoid biopsies from 15 cirrhotic patients and 22 controls by analyzing transcription of genes involved in glutathione and uric acid metabolism using quantitative real-time polymerase chain reaction. Protein levels of glutathione and glutathione disulphide were measured and the glutathione/glutathione disulphide ratio was calculated as marker of oxidative stress. In addition, intestinal myeloperoxidase and fecal calprotectin were determined. Result: Gene transcription of glutathione synthetase and glutathione reductase were significantly different in duodenal and sigmoid biopsies of cirrhotic patients vs. controls, but no alterations were found for other genes nor for glutathione, glutathione disulphide, glutathione/glutathione disulphide ratio and intestinal myeloperoxidase and fecal calprotectin concentrations. Conclusion: This study did not find indications for oxidative stress and low-grade inflammation in the small and large intestine of stable compensated cirrhotic patients. Although these preliminary findings need further validation, we found intestinal oxidative stress not to be a major mechanism contributing to epithelial barrier dysfunction in patients with compensated cirrhosis.",
keywords = "Intestine, Epithelial barrier, Glutathione, Inflammation, BACTERIAL TRANSLOCATION, BARRIER DYSFUNCTION, MUCOSAL ALTERATIONS, NITRIC-OXIDE, PERMEABILITY, INFLAMMATION, RATS, COMPLICATIONS, ANTIOXIDANTS, DISRUPTION",
author = "Kirsten Pijls and Daisy Jonkers and {Elizalde Vilalta}, Montserrat and {Drittij - Reijnders}, {Marie Jose} and Guido Haenen and Aalt Bast and Ad Masclee and Ger Koek",
year = "2016",
doi = "10.5604/16652681.1198816",
language = "English",
volume = "15",
pages = "402--409",
journal = "Annals of Hepatology",
issn = "1665-2681",
publisher = "Mexican Association of Hepatology",
number = "3",

}

TY - JOUR

T1 - Is intestinal oxidative stress involved in patients with compensated liver cirrhosis?

AU - Pijls, Kirsten

AU - Jonkers, Daisy

AU - Elizalde Vilalta, Montserrat

AU - Drittij - Reijnders, Marie Jose

AU - Haenen, Guido

AU - Bast, Aalt

AU - Masclee, Ad

AU - Koek, Ger

PY - 2016

Y1 - 2016

N2 - Background: Liver cirrhosis is associated with intestinal epithelial barrier dysfunction, which may be affected by oxidative stress. Studies in cirrhotic rats provided evidence for intestinal oxidative stress, but studies in cirrhotic patients are scarce. We have shown intestinal barrier dysfunction in patients with compensated cirrhosis. AIM: The present study aimed to investigate whether oxidative stress occurs in the intestinal mucosa of compensated cirrhotic patients and may contribute to barrier dysfunction. Material and methods: Oxidative stress was studied in duodenal and sigmoid biopsies from 15 cirrhotic patients and 22 controls by analyzing transcription of genes involved in glutathione and uric acid metabolism using quantitative real-time polymerase chain reaction. Protein levels of glutathione and glutathione disulphide were measured and the glutathione/glutathione disulphide ratio was calculated as marker of oxidative stress. In addition, intestinal myeloperoxidase and fecal calprotectin were determined. Result: Gene transcription of glutathione synthetase and glutathione reductase were significantly different in duodenal and sigmoid biopsies of cirrhotic patients vs. controls, but no alterations were found for other genes nor for glutathione, glutathione disulphide, glutathione/glutathione disulphide ratio and intestinal myeloperoxidase and fecal calprotectin concentrations. Conclusion: This study did not find indications for oxidative stress and low-grade inflammation in the small and large intestine of stable compensated cirrhotic patients. Although these preliminary findings need further validation, we found intestinal oxidative stress not to be a major mechanism contributing to epithelial barrier dysfunction in patients with compensated cirrhosis.

AB - Background: Liver cirrhosis is associated with intestinal epithelial barrier dysfunction, which may be affected by oxidative stress. Studies in cirrhotic rats provided evidence for intestinal oxidative stress, but studies in cirrhotic patients are scarce. We have shown intestinal barrier dysfunction in patients with compensated cirrhosis. AIM: The present study aimed to investigate whether oxidative stress occurs in the intestinal mucosa of compensated cirrhotic patients and may contribute to barrier dysfunction. Material and methods: Oxidative stress was studied in duodenal and sigmoid biopsies from 15 cirrhotic patients and 22 controls by analyzing transcription of genes involved in glutathione and uric acid metabolism using quantitative real-time polymerase chain reaction. Protein levels of glutathione and glutathione disulphide were measured and the glutathione/glutathione disulphide ratio was calculated as marker of oxidative stress. In addition, intestinal myeloperoxidase and fecal calprotectin were determined. Result: Gene transcription of glutathione synthetase and glutathione reductase were significantly different in duodenal and sigmoid biopsies of cirrhotic patients vs. controls, but no alterations were found for other genes nor for glutathione, glutathione disulphide, glutathione/glutathione disulphide ratio and intestinal myeloperoxidase and fecal calprotectin concentrations. Conclusion: This study did not find indications for oxidative stress and low-grade inflammation in the small and large intestine of stable compensated cirrhotic patients. Although these preliminary findings need further validation, we found intestinal oxidative stress not to be a major mechanism contributing to epithelial barrier dysfunction in patients with compensated cirrhosis.

KW - Intestine

KW - Epithelial barrier

KW - Glutathione

KW - Inflammation

KW - BACTERIAL TRANSLOCATION

KW - BARRIER DYSFUNCTION

KW - MUCOSAL ALTERATIONS

KW - NITRIC-OXIDE

KW - PERMEABILITY

KW - INFLAMMATION

KW - RATS

KW - COMPLICATIONS

KW - ANTIOXIDANTS

KW - DISRUPTION

U2 - 10.5604/16652681.1198816

DO - 10.5604/16652681.1198816

M3 - Article

VL - 15

SP - 402

EP - 409

JO - Annals of Hepatology

JF - Annals of Hepatology

SN - 1665-2681

IS - 3

ER -