Effects of indomethacin, with vitamin A or β-carotene, on the rat gastric mucosa

Extra- and intracellular membrane-bound ATP mechanisms

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3 Citations (Scopus)

Abstract

Background. Indomethacin (IND) is a widely used non-steroidal anti- inflammatory agent in the treatment of various inflammatory disorders, which causes gastrointestinal injury in humans and animal experiments. Vitamin A and β-carotene prevent the IND-induced gastric mucosal injury. These compounds modify the membrane-bound ATP-dependent energy systems. The aims of this investigation were: (1) To study the IND-induced gastric mucosal damage and its prevention by vitamin A and β-carotene; (2) to measure the biochemical compounds of the gastric mucosa {ATP, ADP, ATP/ADP, AMP, ATP+ADP+AMP, 'energy charge' (ATP + 0.5 ADP)/(ATP+ADP+AMP), cAMP, lactate} under the circumstances mentioned above; (3) to analyze the extra- and intracellular regulatory mechanisms between the membrane-bound ATP-dependent energy systems. Methods. The observations were carried out with CFY (Sprague- Dawstrein rats, weighing 180-210 g). The gastric mucosal damage was produced by IND (20 mg/kg sc. administration) and it was prevented by vitamin A (or β-carotene), given in doses of 0.01-0.1 to 1.0-10.0 mg/kg ig. Different biochemical compounds (ATP, ADP, AMP, cAMP, lactate) and parameters (ATP/ADP, adenylate pool, 'energy charge') were measured and calculated. Results. (1) Vitamin A and β-carotene prevented dose-dependently the IND-induced gastric mucosal damage; (2) the extent of ATP-ADP transformation was increased significantly, while the ATP-cAMP decreased in the gastric mucosa after IND- treatment; (3) vitamin A and β-carotene enhanced the extent of ATP-cAMP transformation, while the ATP-ADP transformation was inhibited (the actions were dose-dependent responses); (4) No change was found in 'energy charge' by IND, while its value decreased significantly with vitamin A and β-carotene. Conclusions. (1) A very complex extra- and intracellular feedback mechanism system exists in the gastric mucosa during IND, IND + vitamin A, and IND + β-carotene treatments; (2) The gastric mucosal preventive effect of vitamin A and β-carotene only partly depend on their scavenger properties.

Original languageEnglish
Pages (from-to)287-295
Number of pages9
JournalInflammopharmacology
Volume7
Issue number3
Publication statusPublished - 1999

Fingerprint

Intracellular Membranes
Carotenoids
Gastric Mucosa
Vitamin A
Indomethacin
Adenosine Triphosphate
Adenosine Diphosphate
Adenosine Monophosphate
Stomach
Lactic Acid
Membranes
Wounds and Injuries
Non-Steroidal Anti-Inflammatory Agents

Keywords

  • β-carotene
  • Adenosine nucleotides
  • Cellular energy systems
  • Gastric mucosal injury and prevention
  • Indomethacin
  • Vitamin A

ASJC Scopus subject areas

  • Pharmacology
  • Immunology

Cite this

@article{c12ea8a4fc634dc38566f8d014c7a942,
title = "Effects of indomethacin, with vitamin A or β-carotene, on the rat gastric mucosa: Extra- and intracellular membrane-bound ATP mechanisms",
abstract = "Background. Indomethacin (IND) is a widely used non-steroidal anti- inflammatory agent in the treatment of various inflammatory disorders, which causes gastrointestinal injury in humans and animal experiments. Vitamin A and β-carotene prevent the IND-induced gastric mucosal injury. These compounds modify the membrane-bound ATP-dependent energy systems. The aims of this investigation were: (1) To study the IND-induced gastric mucosal damage and its prevention by vitamin A and β-carotene; (2) to measure the biochemical compounds of the gastric mucosa {ATP, ADP, ATP/ADP, AMP, ATP+ADP+AMP, 'energy charge' (ATP + 0.5 ADP)/(ATP+ADP+AMP), cAMP, lactate} under the circumstances mentioned above; (3) to analyze the extra- and intracellular regulatory mechanisms between the membrane-bound ATP-dependent energy systems. Methods. The observations were carried out with CFY (Sprague- Dawstrein rats, weighing 180-210 g). The gastric mucosal damage was produced by IND (20 mg/kg sc. administration) and it was prevented by vitamin A (or β-carotene), given in doses of 0.01-0.1 to 1.0-10.0 mg/kg ig. Different biochemical compounds (ATP, ADP, AMP, cAMP, lactate) and parameters (ATP/ADP, adenylate pool, 'energy charge') were measured and calculated. Results. (1) Vitamin A and β-carotene prevented dose-dependently the IND-induced gastric mucosal damage; (2) the extent of ATP-ADP transformation was increased significantly, while the ATP-cAMP decreased in the gastric mucosa after IND- treatment; (3) vitamin A and β-carotene enhanced the extent of ATP-cAMP transformation, while the ATP-ADP transformation was inhibited (the actions were dose-dependent responses); (4) No change was found in 'energy charge' by IND, while its value decreased significantly with vitamin A and β-carotene. Conclusions. (1) A very complex extra- and intracellular feedback mechanism system exists in the gastric mucosa during IND, IND + vitamin A, and IND + β-carotene treatments; (2) The gastric mucosal preventive effect of vitamin A and β-carotene only partly depend on their scavenger properties.",
keywords = "β-carotene, Adenosine nucleotides, Cellular energy systems, Gastric mucosal injury and prevention, Indomethacin, Vitamin A",
author = "G. M{\'o}zsik and G. Rumi and B. Bodis and M. Figler and A. Kiraly and G. S{\"u}t{\"o} and A. Vincze",
year = "1999",
language = "English",
volume = "7",
pages = "287--295",
journal = "Inflammopharmacology",
issn = "0925-4692",
publisher = "Birkhauser Verlag Basel",
number = "3",

}

TY - JOUR

T1 - Effects of indomethacin, with vitamin A or β-carotene, on the rat gastric mucosa

T2 - Extra- and intracellular membrane-bound ATP mechanisms

AU - Mózsik, G.

AU - Rumi, G.

AU - Bodis, B.

AU - Figler, M.

AU - Kiraly, A.

AU - Sütö, G.

AU - Vincze, A.

PY - 1999

Y1 - 1999

N2 - Background. Indomethacin (IND) is a widely used non-steroidal anti- inflammatory agent in the treatment of various inflammatory disorders, which causes gastrointestinal injury in humans and animal experiments. Vitamin A and β-carotene prevent the IND-induced gastric mucosal injury. These compounds modify the membrane-bound ATP-dependent energy systems. The aims of this investigation were: (1) To study the IND-induced gastric mucosal damage and its prevention by vitamin A and β-carotene; (2) to measure the biochemical compounds of the gastric mucosa {ATP, ADP, ATP/ADP, AMP, ATP+ADP+AMP, 'energy charge' (ATP + 0.5 ADP)/(ATP+ADP+AMP), cAMP, lactate} under the circumstances mentioned above; (3) to analyze the extra- and intracellular regulatory mechanisms between the membrane-bound ATP-dependent energy systems. Methods. The observations were carried out with CFY (Sprague- Dawstrein rats, weighing 180-210 g). The gastric mucosal damage was produced by IND (20 mg/kg sc. administration) and it was prevented by vitamin A (or β-carotene), given in doses of 0.01-0.1 to 1.0-10.0 mg/kg ig. Different biochemical compounds (ATP, ADP, AMP, cAMP, lactate) and parameters (ATP/ADP, adenylate pool, 'energy charge') were measured and calculated. Results. (1) Vitamin A and β-carotene prevented dose-dependently the IND-induced gastric mucosal damage; (2) the extent of ATP-ADP transformation was increased significantly, while the ATP-cAMP decreased in the gastric mucosa after IND- treatment; (3) vitamin A and β-carotene enhanced the extent of ATP-cAMP transformation, while the ATP-ADP transformation was inhibited (the actions were dose-dependent responses); (4) No change was found in 'energy charge' by IND, while its value decreased significantly with vitamin A and β-carotene. Conclusions. (1) A very complex extra- and intracellular feedback mechanism system exists in the gastric mucosa during IND, IND + vitamin A, and IND + β-carotene treatments; (2) The gastric mucosal preventive effect of vitamin A and β-carotene only partly depend on their scavenger properties.

AB - Background. Indomethacin (IND) is a widely used non-steroidal anti- inflammatory agent in the treatment of various inflammatory disorders, which causes gastrointestinal injury in humans and animal experiments. Vitamin A and β-carotene prevent the IND-induced gastric mucosal injury. These compounds modify the membrane-bound ATP-dependent energy systems. The aims of this investigation were: (1) To study the IND-induced gastric mucosal damage and its prevention by vitamin A and β-carotene; (2) to measure the biochemical compounds of the gastric mucosa {ATP, ADP, ATP/ADP, AMP, ATP+ADP+AMP, 'energy charge' (ATP + 0.5 ADP)/(ATP+ADP+AMP), cAMP, lactate} under the circumstances mentioned above; (3) to analyze the extra- and intracellular regulatory mechanisms between the membrane-bound ATP-dependent energy systems. Methods. The observations were carried out with CFY (Sprague- Dawstrein rats, weighing 180-210 g). The gastric mucosal damage was produced by IND (20 mg/kg sc. administration) and it was prevented by vitamin A (or β-carotene), given in doses of 0.01-0.1 to 1.0-10.0 mg/kg ig. Different biochemical compounds (ATP, ADP, AMP, cAMP, lactate) and parameters (ATP/ADP, adenylate pool, 'energy charge') were measured and calculated. Results. (1) Vitamin A and β-carotene prevented dose-dependently the IND-induced gastric mucosal damage; (2) the extent of ATP-ADP transformation was increased significantly, while the ATP-cAMP decreased in the gastric mucosa after IND- treatment; (3) vitamin A and β-carotene enhanced the extent of ATP-cAMP transformation, while the ATP-ADP transformation was inhibited (the actions were dose-dependent responses); (4) No change was found in 'energy charge' by IND, while its value decreased significantly with vitamin A and β-carotene. Conclusions. (1) A very complex extra- and intracellular feedback mechanism system exists in the gastric mucosa during IND, IND + vitamin A, and IND + β-carotene treatments; (2) The gastric mucosal preventive effect of vitamin A and β-carotene only partly depend on their scavenger properties.

KW - β-carotene

KW - Adenosine nucleotides

KW - Cellular energy systems

KW - Gastric mucosal injury and prevention

KW - Indomethacin

KW - Vitamin A

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M3 - Article

VL - 7

SP - 287

EP - 295

JO - Inflammopharmacology

JF - Inflammopharmacology

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