The interrelationships between the lipid peroxidation, superoxide dismutase activity, development of gastric H+ secretion and gastric mucosal damage produced by intragastric administration of aspirin in pylorus-ligated rats

B. Czegledi, T. Javor, L. Nagy, I. Patty, A. Tigyi, F. Tarnok, T. Zsoldos, G. Mózsik

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Gastric mucosal damage of pylorus-ligated rats was induced by the intragastric administration of aspirin at 200 mg/kg at the time of ligation. The animals were sacrified at 0, 1, 2, 3, and 4 h after the treatment. The gastric lesions (ulcers) were counted and their severities were calculated, and the volume of gastric secretion and the H+ output were measured. The extent of lipid peroxidation was assessed by measuring the malondialdehyde (MDA) in the gastric mucosa, simultaneously with measurement of the activity of superoxide dismutase (SOD). It was found in these pylorus-ligated rats that: i) the number of visible gastric lesions was significantly higher 1 h after aspirin administration than at other times; ii) the severity of gastric lesions increased significanlty at the 3rd and 4th hour after administration of aspirin; iii) the volume of gastric secretory responses increased gradually after administration of aspirin and to a higher extent than the H+ output; iv) the H+ output was significantly less after aspirin administration than that after pylorus ligation only; v) the gastric mucosal SOD activity significantly increased 1 h after administration of aspirin, decreasing significantly and gradually thereafter; vi) the tissue level of MDA remained unchanged 1 h after aspirin administration, decreasing significantly thereafter. It can be concluded that: i) the significant increase in the SOD activity is associated with a significant increase of gastric mucosal damage in aspirin-treated pylorus-ligated rats; ii) no active gastric H+ secretion can be demonstrated at the peak times of gastric mucosal damage produced by aspirin; iii) the existence of gastric H+ backdiffusion can be proved during the first 2 hours after pyloric ligation plus aspirin treatment; iv) the significant increase of the fundic mucosal SOD activity may represent one of the defence mechanisms against the aspirin exposition in the stomach of the rat.

Original languageEnglish
Pages (from-to)23-30
Number of pages8
JournalInternational Journal of Tissue Reactions
Volume8
Issue number1
Publication statusPublished - 1986

Fingerprint

Pylorus
Lipid Peroxidation
Aspirin
Superoxide Dismutase
Stomach
Ligation
Malondialdehyde
Stomach Ulcer
Gastric Mucosa

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

Cite this

@article{4a68c353aaa34ada9ce8770769b4c0ca,
title = "The interrelationships between the lipid peroxidation, superoxide dismutase activity, development of gastric H+ secretion and gastric mucosal damage produced by intragastric administration of aspirin in pylorus-ligated rats",
abstract = "Gastric mucosal damage of pylorus-ligated rats was induced by the intragastric administration of aspirin at 200 mg/kg at the time of ligation. The animals were sacrified at 0, 1, 2, 3, and 4 h after the treatment. The gastric lesions (ulcers) were counted and their severities were calculated, and the volume of gastric secretion and the H+ output were measured. The extent of lipid peroxidation was assessed by measuring the malondialdehyde (MDA) in the gastric mucosa, simultaneously with measurement of the activity of superoxide dismutase (SOD). It was found in these pylorus-ligated rats that: i) the number of visible gastric lesions was significantly higher 1 h after aspirin administration than at other times; ii) the severity of gastric lesions increased significanlty at the 3rd and 4th hour after administration of aspirin; iii) the volume of gastric secretory responses increased gradually after administration of aspirin and to a higher extent than the H+ output; iv) the H+ output was significantly less after aspirin administration than that after pylorus ligation only; v) the gastric mucosal SOD activity significantly increased 1 h after administration of aspirin, decreasing significantly and gradually thereafter; vi) the tissue level of MDA remained unchanged 1 h after aspirin administration, decreasing significantly thereafter. It can be concluded that: i) the significant increase in the SOD activity is associated with a significant increase of gastric mucosal damage in aspirin-treated pylorus-ligated rats; ii) no active gastric H+ secretion can be demonstrated at the peak times of gastric mucosal damage produced by aspirin; iii) the existence of gastric H+ backdiffusion can be proved during the first 2 hours after pyloric ligation plus aspirin treatment; iv) the significant increase of the fundic mucosal SOD activity may represent one of the defence mechanisms against the aspirin exposition in the stomach of the rat.",
author = "B. Czegledi and T. Javor and L. Nagy and I. Patty and A. Tigyi and F. Tarnok and T. Zsoldos and G. M{\'o}zsik",
year = "1986",
language = "English",
volume = "8",
pages = "23--30",
journal = "International Journal of Tissue Reactions",
issn = "0250-0868",
publisher = "Bioscience Ediprint Inc.",
number = "1",

}

TY - JOUR

T1 - The interrelationships between the lipid peroxidation, superoxide dismutase activity, development of gastric H+ secretion and gastric mucosal damage produced by intragastric administration of aspirin in pylorus-ligated rats

AU - Czegledi, B.

AU - Javor, T.

AU - Nagy, L.

AU - Patty, I.

AU - Tigyi, A.

AU - Tarnok, F.

AU - Zsoldos, T.

AU - Mózsik, G.

PY - 1986

Y1 - 1986

N2 - Gastric mucosal damage of pylorus-ligated rats was induced by the intragastric administration of aspirin at 200 mg/kg at the time of ligation. The animals were sacrified at 0, 1, 2, 3, and 4 h after the treatment. The gastric lesions (ulcers) were counted and their severities were calculated, and the volume of gastric secretion and the H+ output were measured. The extent of lipid peroxidation was assessed by measuring the malondialdehyde (MDA) in the gastric mucosa, simultaneously with measurement of the activity of superoxide dismutase (SOD). It was found in these pylorus-ligated rats that: i) the number of visible gastric lesions was significantly higher 1 h after aspirin administration than at other times; ii) the severity of gastric lesions increased significanlty at the 3rd and 4th hour after administration of aspirin; iii) the volume of gastric secretory responses increased gradually after administration of aspirin and to a higher extent than the H+ output; iv) the H+ output was significantly less after aspirin administration than that after pylorus ligation only; v) the gastric mucosal SOD activity significantly increased 1 h after administration of aspirin, decreasing significantly and gradually thereafter; vi) the tissue level of MDA remained unchanged 1 h after aspirin administration, decreasing significantly thereafter. It can be concluded that: i) the significant increase in the SOD activity is associated with a significant increase of gastric mucosal damage in aspirin-treated pylorus-ligated rats; ii) no active gastric H+ secretion can be demonstrated at the peak times of gastric mucosal damage produced by aspirin; iii) the existence of gastric H+ backdiffusion can be proved during the first 2 hours after pyloric ligation plus aspirin treatment; iv) the significant increase of the fundic mucosal SOD activity may represent one of the defence mechanisms against the aspirin exposition in the stomach of the rat.

AB - Gastric mucosal damage of pylorus-ligated rats was induced by the intragastric administration of aspirin at 200 mg/kg at the time of ligation. The animals were sacrified at 0, 1, 2, 3, and 4 h after the treatment. The gastric lesions (ulcers) were counted and their severities were calculated, and the volume of gastric secretion and the H+ output were measured. The extent of lipid peroxidation was assessed by measuring the malondialdehyde (MDA) in the gastric mucosa, simultaneously with measurement of the activity of superoxide dismutase (SOD). It was found in these pylorus-ligated rats that: i) the number of visible gastric lesions was significantly higher 1 h after aspirin administration than at other times; ii) the severity of gastric lesions increased significanlty at the 3rd and 4th hour after administration of aspirin; iii) the volume of gastric secretory responses increased gradually after administration of aspirin and to a higher extent than the H+ output; iv) the H+ output was significantly less after aspirin administration than that after pylorus ligation only; v) the gastric mucosal SOD activity significantly increased 1 h after administration of aspirin, decreasing significantly and gradually thereafter; vi) the tissue level of MDA remained unchanged 1 h after aspirin administration, decreasing significantly thereafter. It can be concluded that: i) the significant increase in the SOD activity is associated with a significant increase of gastric mucosal damage in aspirin-treated pylorus-ligated rats; ii) no active gastric H+ secretion can be demonstrated at the peak times of gastric mucosal damage produced by aspirin; iii) the existence of gastric H+ backdiffusion can be proved during the first 2 hours after pyloric ligation plus aspirin treatment; iv) the significant increase of the fundic mucosal SOD activity may represent one of the defence mechanisms against the aspirin exposition in the stomach of the rat.

UR - http://www.scopus.com/inward/record.url?scp=0022655865&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022655865&partnerID=8YFLogxK

M3 - Article

VL - 8

SP - 23

EP - 30

JO - International Journal of Tissue Reactions

JF - International Journal of Tissue Reactions

SN - 0250-0868

IS - 1

ER -