Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport

S. Selim Karayalcin, Christopher W. Sturbaum, Joseph T. Wachsman, Jih Ho Cha, Don W. Powell

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

The changes in short circuit current (electrogenic Cl- secretion) of rat colon brought about by xanthine/xanthine oxidase in the Ussing chamber were inhibited by catalase and diethyldithiocarbamate, but not by superoxide dismutase. These results, the reproduction of the response with glucose/glucose oxidase and with exogenous H2O2, and the lack of effect of preincubation with deferoxamine or thiourea implicate H2O2, and not O2 -• or OH, as the important reactive oxygen metabolite altering intestinal electrolyte transport. 1 mM H2O2 stimulated colonic PGE2 and PGE2 production 8- and 15-fold, respectively, inhibited neutral NaCl absorption, and stimulated biphasic electrogenic Cl secretion with little effect on enterocyte lactic dehydrogenase release, epithelial conductance, or histology. Cl- secretion was reduced by cyclooxygenase inhibition. Also, the Cl- secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine. Thus, H2O2 appears to alter electrolyte transport by releasing prostaglandins that activate the enteric nervous system. The change in short circuit current in response to Iloprost, but not PGE2, was blocked by tetrodotoxin. Therefore, PGI2 may be the mediator of the H2O2 response. H2O2 produced in nontoxic concentrations in the inflamed gut could have significant physiologic effects on intestinal water and electrolyte transport.

Original languageEnglish (US)
Pages (from-to)60-68
Number of pages9
JournalJournal of Clinical Investigation
Volume86
Issue number1
StatePublished - Jul 1990
Externally publishedYes

Fingerprint

Dinoprostone
Hydrogen Peroxide
Electrolytes
Prostaglandins
Enteric Nervous System
Tetrodotoxin
Iloprost
Ditiocarb
Thiourea
Hexamethonium
Glucose Oxidase
Xanthine
Deferoxamine
Enterocytes
Xanthine Oxidase
Epoprostenol
Prostaglandin-Endoperoxide Synthases
Atropine
Catalase
Superoxide Dismutase

Keywords

  • Enteric nervous system
  • Inflammation
  • Intestinal secretion
  • Oxygen radical
  • Prostaglandin

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Karayalcin, S. S., Sturbaum, C. W., Wachsman, J. T., Cha, J. H., & Powell, D. W. (1990). Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport. Journal of Clinical Investigation, 86(1), 60-68.

Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport. / Karayalcin, S. Selim; Sturbaum, Christopher W.; Wachsman, Joseph T.; Cha, Jih Ho; Powell, Don W.

In: Journal of Clinical Investigation, Vol. 86, No. 1, 07.1990, p. 60-68.

Research output: Contribution to journalArticle

Karayalcin, SS, Sturbaum, CW, Wachsman, JT, Cha, JH & Powell, DW 1990, 'Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport', Journal of Clinical Investigation, vol. 86, no. 1, pp. 60-68.
Karayalcin, S. Selim ; Sturbaum, Christopher W. ; Wachsman, Joseph T. ; Cha, Jih Ho ; Powell, Don W. / Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport. In: Journal of Clinical Investigation. 1990 ; Vol. 86, No. 1. pp. 60-68.
@article{364013c2896e4574b43b8671141879d5,
title = "Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport",
abstract = "The changes in short circuit current (electrogenic Cl- secretion) of rat colon brought about by xanthine/xanthine oxidase in the Ussing chamber were inhibited by catalase and diethyldithiocarbamate, but not by superoxide dismutase. These results, the reproduction of the response with glucose/glucose oxidase and with exogenous H2O2, and the lack of effect of preincubation with deferoxamine or thiourea implicate H2O2, and not O2 -• or OH•, as the important reactive oxygen metabolite altering intestinal electrolyte transport. 1 mM H2O2 stimulated colonic PGE2 and PGE2 production 8- and 15-fold, respectively, inhibited neutral NaCl absorption, and stimulated biphasic electrogenic Cl secretion with little effect on enterocyte lactic dehydrogenase release, epithelial conductance, or histology. Cl- secretion was reduced by cyclooxygenase inhibition. Also, the Cl- secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine. Thus, H2O2 appears to alter electrolyte transport by releasing prostaglandins that activate the enteric nervous system. The change in short circuit current in response to Iloprost, but not PGE2, was blocked by tetrodotoxin. Therefore, PGI2 may be the mediator of the H2O2 response. H2O2 produced in nontoxic concentrations in the inflamed gut could have significant physiologic effects on intestinal water and electrolyte transport.",
keywords = "Enteric nervous system, Inflammation, Intestinal secretion, Oxygen radical, Prostaglandin",
author = "Karayalcin, {S. Selim} and Sturbaum, {Christopher W.} and Wachsman, {Joseph T.} and Cha, {Jih Ho} and Powell, {Don W.}",
year = "1990",
month = "7",
language = "English (US)",
volume = "86",
pages = "60--68",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "1",

}

TY - JOUR

T1 - Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport

AU - Karayalcin, S. Selim

AU - Sturbaum, Christopher W.

AU - Wachsman, Joseph T.

AU - Cha, Jih Ho

AU - Powell, Don W.

PY - 1990/7

Y1 - 1990/7

N2 - The changes in short circuit current (electrogenic Cl- secretion) of rat colon brought about by xanthine/xanthine oxidase in the Ussing chamber were inhibited by catalase and diethyldithiocarbamate, but not by superoxide dismutase. These results, the reproduction of the response with glucose/glucose oxidase and with exogenous H2O2, and the lack of effect of preincubation with deferoxamine or thiourea implicate H2O2, and not O2 -• or OH•, as the important reactive oxygen metabolite altering intestinal electrolyte transport. 1 mM H2O2 stimulated colonic PGE2 and PGE2 production 8- and 15-fold, respectively, inhibited neutral NaCl absorption, and stimulated biphasic electrogenic Cl secretion with little effect on enterocyte lactic dehydrogenase release, epithelial conductance, or histology. Cl- secretion was reduced by cyclooxygenase inhibition. Also, the Cl- secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine. Thus, H2O2 appears to alter electrolyte transport by releasing prostaglandins that activate the enteric nervous system. The change in short circuit current in response to Iloprost, but not PGE2, was blocked by tetrodotoxin. Therefore, PGI2 may be the mediator of the H2O2 response. H2O2 produced in nontoxic concentrations in the inflamed gut could have significant physiologic effects on intestinal water and electrolyte transport.

AB - The changes in short circuit current (electrogenic Cl- secretion) of rat colon brought about by xanthine/xanthine oxidase in the Ussing chamber were inhibited by catalase and diethyldithiocarbamate, but not by superoxide dismutase. These results, the reproduction of the response with glucose/glucose oxidase and with exogenous H2O2, and the lack of effect of preincubation with deferoxamine or thiourea implicate H2O2, and not O2 -• or OH•, as the important reactive oxygen metabolite altering intestinal electrolyte transport. 1 mM H2O2 stimulated colonic PGE2 and PGE2 production 8- and 15-fold, respectively, inhibited neutral NaCl absorption, and stimulated biphasic electrogenic Cl secretion with little effect on enterocyte lactic dehydrogenase release, epithelial conductance, or histology. Cl- secretion was reduced by cyclooxygenase inhibition. Also, the Cl- secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine. Thus, H2O2 appears to alter electrolyte transport by releasing prostaglandins that activate the enteric nervous system. The change in short circuit current in response to Iloprost, but not PGE2, was blocked by tetrodotoxin. Therefore, PGI2 may be the mediator of the H2O2 response. H2O2 produced in nontoxic concentrations in the inflamed gut could have significant physiologic effects on intestinal water and electrolyte transport.

KW - Enteric nervous system

KW - Inflammation

KW - Intestinal secretion

KW - Oxygen radical

KW - Prostaglandin

UR - http://www.scopus.com/inward/record.url?scp=0025358713&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025358713&partnerID=8YFLogxK

M3 - Article

VL - 86

SP - 60

EP - 68

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 1

ER -