Superoxide

A critical oxygen-free radical in ischemic bowel injury

Stephen P. Dunn, Kirby R. Gross, Michael Dalsing, Richard Hon, Jay L. Grosfeld

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (O), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment 1 treatment animals (n=20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n=71) received Ringer's lactate alone. Experiment II treatment animals (n=16) received 1 cc of 100% DMSO gavage, and control animals (n=11) received no treatment. Experiment III treatment animals (n=17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n=11) received nothing. Experiment IV treatment animals (n=14) received 300 μg of sodium selenate by gavage dissolved in deionized water, and control animals (n=15) receiving nothing. Experiment V treatment animals (n=20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n=20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using χ2 analysis. SOD increased survival (P<.05) and length of survival (P<.02) and decreased the perforation rate (P<.025) in animals subject to ischemic bowell injury. CAT, DMSO, and selenium treatment were not beneficial. These data suggest a critical role for superoxide anion in the pathogenesis of intestinal ischemia.

Original languageEnglish
Pages (from-to)740-744
Number of pages5
JournalJournal of Pediatric Surgery
Volume19
Issue number6
DOIs
StatePublished - 1984
Externally publishedYes

Fingerprint

Superoxides
Free Radicals
Reactive Oxygen Species
Wounds and Injuries
Selenium
Dimethyl Sulfoxide
Catalase
Superoxide Dismutase
Ischemia
Selenic Acid
Diet
Superior Mesenteric Artery
Surgical Instruments
Hydroxyl Radical
Hydrogen Peroxide
Anions
Sprague Dawley Rats
Necrosis
Phosphates
Oxygen

Keywords

  • catalase
  • dimethyl sulfoxide
  • Ischemic bowel
  • oxygen-free radicals
  • selenium
  • superoxide dismutase

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Surgery

Cite this

Superoxide : A critical oxygen-free radical in ischemic bowel injury. / Dunn, Stephen P.; Gross, Kirby R.; Dalsing, Michael; Hon, Richard; Grosfeld, Jay L.

In: Journal of Pediatric Surgery, Vol. 19, No. 6, 1984, p. 740-744.

Research output: Contribution to journalArticle

Dunn, Stephen P. ; Gross, Kirby R. ; Dalsing, Michael ; Hon, Richard ; Grosfeld, Jay L. / Superoxide : A critical oxygen-free radical in ischemic bowel injury. In: Journal of Pediatric Surgery. 1984 ; Vol. 19, No. 6. pp. 740-744.
@article{3c54ce12acb44781833f7bacd36024a5,
title = "Superoxide: A critical oxygen-free radical in ischemic bowel injury",
abstract = "The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (O), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment 1 treatment animals (n=20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n=71) received Ringer's lactate alone. Experiment II treatment animals (n=16) received 1 cc of 100{\%} DMSO gavage, and control animals (n=11) received no treatment. Experiment III treatment animals (n=17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n=11) received nothing. Experiment IV treatment animals (n=14) received 300 μg of sodium selenate by gavage dissolved in deionized water, and control animals (n=15) receiving nothing. Experiment V treatment animals (n=20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n=20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using χ2 analysis. SOD increased survival (P<.05) and length of survival (P<.02) and decreased the perforation rate (P<.025) in animals subject to ischemic bowell injury. CAT, DMSO, and selenium treatment were not beneficial. These data suggest a critical role for superoxide anion in the pathogenesis of intestinal ischemia.",
keywords = "catalase, dimethyl sulfoxide, Ischemic bowel, oxygen-free radicals, selenium, superoxide dismutase",
author = "Dunn, {Stephen P.} and Gross, {Kirby R.} and Michael Dalsing and Richard Hon and Grosfeld, {Jay L.}",
year = "1984",
doi = "10.1016/S0022-3468(84)80361-9",
language = "English",
volume = "19",
pages = "740--744",
journal = "Journal of Pediatric Surgery",
issn = "0022-3468",
publisher = "W.B. Saunders Ltd",
number = "6",

}

TY - JOUR

T1 - Superoxide

T2 - A critical oxygen-free radical in ischemic bowel injury

AU - Dunn, Stephen P.

AU - Gross, Kirby R.

AU - Dalsing, Michael

AU - Hon, Richard

AU - Grosfeld, Jay L.

PY - 1984

Y1 - 1984

N2 - The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (O), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment 1 treatment animals (n=20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n=71) received Ringer's lactate alone. Experiment II treatment animals (n=16) received 1 cc of 100% DMSO gavage, and control animals (n=11) received no treatment. Experiment III treatment animals (n=17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n=11) received nothing. Experiment IV treatment animals (n=14) received 300 μg of sodium selenate by gavage dissolved in deionized water, and control animals (n=15) receiving nothing. Experiment V treatment animals (n=20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n=20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using χ2 analysis. SOD increased survival (P<.05) and length of survival (P<.02) and decreased the perforation rate (P<.025) in animals subject to ischemic bowell injury. CAT, DMSO, and selenium treatment were not beneficial. These data suggest a critical role for superoxide anion in the pathogenesis of intestinal ischemia.

AB - The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (O), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment 1 treatment animals (n=20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n=71) received Ringer's lactate alone. Experiment II treatment animals (n=16) received 1 cc of 100% DMSO gavage, and control animals (n=11) received no treatment. Experiment III treatment animals (n=17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n=11) received nothing. Experiment IV treatment animals (n=14) received 300 μg of sodium selenate by gavage dissolved in deionized water, and control animals (n=15) receiving nothing. Experiment V treatment animals (n=20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n=20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using χ2 analysis. SOD increased survival (P<.05) and length of survival (P<.02) and decreased the perforation rate (P<.025) in animals subject to ischemic bowell injury. CAT, DMSO, and selenium treatment were not beneficial. These data suggest a critical role for superoxide anion in the pathogenesis of intestinal ischemia.

KW - catalase

KW - dimethyl sulfoxide

KW - Ischemic bowel

KW - oxygen-free radicals

KW - selenium

KW - superoxide dismutase

UR - http://www.scopus.com/inward/record.url?scp=0021687450&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021687450&partnerID=8YFLogxK

U2 - 10.1016/S0022-3468(84)80361-9

DO - 10.1016/S0022-3468(84)80361-9

M3 - Article

VL - 19

SP - 740

EP - 744

JO - Journal of Pediatric Surgery

JF - Journal of Pediatric Surgery

SN - 0022-3468

IS - 6

ER -