Mechanisms of action of retinoids in gastrointestinal mucosal protection in animals, human healthy subjects and patients

G. Mózsik, Beáta Bódis, M. Figler, Ágnes Király, Oszkár Karádi, A. Pár, G. Rumi, G. Sütö, G. Tóth, A. Vincze

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Retinoids prevent chemically induced gastric mucosal damage without inhibiting gastric acid secretion ("nutritional gastric cytoprotection"). The gastroprotective effects of retinoids do not depend on 1) vitamin A activity; 2) number of unsaturated double bonds; 3) the presence of a characteristic chemical structure of their terminal components; however, they depend on 1) intact vagal nerve and 2) adrenals in experimental animals. The gastric cytoprotective effect of retinoids produces a dose-dependent inhibition of ATP-transformation into ADP. It also increases the transformation of ATP into cAMP. Other features of these gastric cytoprotective effects of retinoids include: 1) The retinoid-induced gastric mucosal protection differs from that of PGs; 2) The cAMP is an intracellular signal in the development of gastric mucosal damage produced by chemicals (e.g., ethanol, HCl, indomethacin) and in the protection of gastric mucosa induced by retinoids (but not by PGs); 3) The gastric mucosal protection induced by retinoids and gastric mucosal permeability can be separated in time. The existence of gastric mucosal protection can be demonstrated in healthy persons (against indomethacin treatment), in patients with gastric ulcer (GU) and duodenal ulcer (DU) without any inhibition of gastric acid secretion. The serum levels of vitamin A and zeaxanthin were significantly decreased in patients with chronic gastrointestinal (GI) inflammatory diseases (e.g., terminal ileitis, ulcerative colitis), colorectal polyposis, and different (e.g., esophageal, gastric, pancreatic, hepatocellular and colorectal) malignant diseases. The serum levels of vitamin A provitamins were unchanged and their GI mucosal protective effects do not depend on vitamin A activity. Conclusions: 1) Abundant experimental and human observations clearly proved the defensive role of retinoids in the GI tract; 2) There is a correlation between the a) scavenger properties of retinoids vs. intact vagal nerve; b) scavenging properties vs. intact adrenals. 3) The GI mucosal protective effect of retinoids is correlated with biochemical changes in the GI mucosa.

Original languageEnglish
Pages (from-to)3103-3112
Number of pages10
JournalLife Sciences
Volume69
Issue number25-26
DOIs
Publication statusPublished - Nov 9 2001

Fingerprint

Retinoids
Stomach
Healthy Volunteers
Animals
Vitamin A
Gastric Acid
Indomethacin
Adenosine Triphosphate
Acids
Cytoprotection
Gastrointestinal Diseases
Scavenging
Stomach Ulcer
Duodenal Ulcer
Gastric Mucosa
Serum
Ulcerative Colitis
Crohn Disease
Adenosine Diphosphate
Gastrointestinal Tract

Keywords

  • ADP
  • ATP
  • cAMP
  • Gastric mucosal damage
  • Gastric mucosal protection
  • Human
  • Retinoids

ASJC Scopus subject areas

  • Pharmacology

Cite this

Mechanisms of action of retinoids in gastrointestinal mucosal protection in animals, human healthy subjects and patients. / Mózsik, G.; Bódis, Beáta; Figler, M.; Király, Ágnes; Karádi, Oszkár; Pár, A.; Rumi, G.; Sütö, G.; Tóth, G.; Vincze, A.

In: Life Sciences, Vol. 69, No. 25-26, 09.11.2001, p. 3103-3112.

Research output: Contribution to journalArticle

@article{e6c3e96c36c74dada39adc1726302ae8,
title = "Mechanisms of action of retinoids in gastrointestinal mucosal protection in animals, human healthy subjects and patients",
abstract = "Retinoids prevent chemically induced gastric mucosal damage without inhibiting gastric acid secretion ({"}nutritional gastric cytoprotection{"}). The gastroprotective effects of retinoids do not depend on 1) vitamin A activity; 2) number of unsaturated double bonds; 3) the presence of a characteristic chemical structure of their terminal components; however, they depend on 1) intact vagal nerve and 2) adrenals in experimental animals. The gastric cytoprotective effect of retinoids produces a dose-dependent inhibition of ATP-transformation into ADP. It also increases the transformation of ATP into cAMP. Other features of these gastric cytoprotective effects of retinoids include: 1) The retinoid-induced gastric mucosal protection differs from that of PGs; 2) The cAMP is an intracellular signal in the development of gastric mucosal damage produced by chemicals (e.g., ethanol, HCl, indomethacin) and in the protection of gastric mucosa induced by retinoids (but not by PGs); 3) The gastric mucosal protection induced by retinoids and gastric mucosal permeability can be separated in time. The existence of gastric mucosal protection can be demonstrated in healthy persons (against indomethacin treatment), in patients with gastric ulcer (GU) and duodenal ulcer (DU) without any inhibition of gastric acid secretion. The serum levels of vitamin A and zeaxanthin were significantly decreased in patients with chronic gastrointestinal (GI) inflammatory diseases (e.g., terminal ileitis, ulcerative colitis), colorectal polyposis, and different (e.g., esophageal, gastric, pancreatic, hepatocellular and colorectal) malignant diseases. The serum levels of vitamin A provitamins were unchanged and their GI mucosal protective effects do not depend on vitamin A activity. Conclusions: 1) Abundant experimental and human observations clearly proved the defensive role of retinoids in the GI tract; 2) There is a correlation between the a) scavenger properties of retinoids vs. intact vagal nerve; b) scavenging properties vs. intact adrenals. 3) The GI mucosal protective effect of retinoids is correlated with biochemical changes in the GI mucosa.",
keywords = "ADP, ATP, cAMP, Gastric mucosal damage, Gastric mucosal protection, Human, Retinoids",
author = "G. M{\'o}zsik and Be{\'a}ta B{\'o}dis and M. Figler and {\'A}gnes Kir{\'a}ly and Oszk{\'a}r Kar{\'a}di and A. P{\'a}r and G. Rumi and G. S{\"u}t{\"o} and G. T{\'o}th and A. Vincze",
year = "2001",
month = "11",
day = "9",
doi = "10.1016/S0024-3205(01)01416-3",
language = "English",
volume = "69",
pages = "3103--3112",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "25-26",

}

TY - JOUR

T1 - Mechanisms of action of retinoids in gastrointestinal mucosal protection in animals, human healthy subjects and patients

AU - Mózsik, G.

AU - Bódis, Beáta

AU - Figler, M.

AU - Király, Ágnes

AU - Karádi, Oszkár

AU - Pár, A.

AU - Rumi, G.

AU - Sütö, G.

AU - Tóth, G.

AU - Vincze, A.

PY - 2001/11/9

Y1 - 2001/11/9

N2 - Retinoids prevent chemically induced gastric mucosal damage without inhibiting gastric acid secretion ("nutritional gastric cytoprotection"). The gastroprotective effects of retinoids do not depend on 1) vitamin A activity; 2) number of unsaturated double bonds; 3) the presence of a characteristic chemical structure of their terminal components; however, they depend on 1) intact vagal nerve and 2) adrenals in experimental animals. The gastric cytoprotective effect of retinoids produces a dose-dependent inhibition of ATP-transformation into ADP. It also increases the transformation of ATP into cAMP. Other features of these gastric cytoprotective effects of retinoids include: 1) The retinoid-induced gastric mucosal protection differs from that of PGs; 2) The cAMP is an intracellular signal in the development of gastric mucosal damage produced by chemicals (e.g., ethanol, HCl, indomethacin) and in the protection of gastric mucosa induced by retinoids (but not by PGs); 3) The gastric mucosal protection induced by retinoids and gastric mucosal permeability can be separated in time. The existence of gastric mucosal protection can be demonstrated in healthy persons (against indomethacin treatment), in patients with gastric ulcer (GU) and duodenal ulcer (DU) without any inhibition of gastric acid secretion. The serum levels of vitamin A and zeaxanthin were significantly decreased in patients with chronic gastrointestinal (GI) inflammatory diseases (e.g., terminal ileitis, ulcerative colitis), colorectal polyposis, and different (e.g., esophageal, gastric, pancreatic, hepatocellular and colorectal) malignant diseases. The serum levels of vitamin A provitamins were unchanged and their GI mucosal protective effects do not depend on vitamin A activity. Conclusions: 1) Abundant experimental and human observations clearly proved the defensive role of retinoids in the GI tract; 2) There is a correlation between the a) scavenger properties of retinoids vs. intact vagal nerve; b) scavenging properties vs. intact adrenals. 3) The GI mucosal protective effect of retinoids is correlated with biochemical changes in the GI mucosa.

AB - Retinoids prevent chemically induced gastric mucosal damage without inhibiting gastric acid secretion ("nutritional gastric cytoprotection"). The gastroprotective effects of retinoids do not depend on 1) vitamin A activity; 2) number of unsaturated double bonds; 3) the presence of a characteristic chemical structure of their terminal components; however, they depend on 1) intact vagal nerve and 2) adrenals in experimental animals. The gastric cytoprotective effect of retinoids produces a dose-dependent inhibition of ATP-transformation into ADP. It also increases the transformation of ATP into cAMP. Other features of these gastric cytoprotective effects of retinoids include: 1) The retinoid-induced gastric mucosal protection differs from that of PGs; 2) The cAMP is an intracellular signal in the development of gastric mucosal damage produced by chemicals (e.g., ethanol, HCl, indomethacin) and in the protection of gastric mucosa induced by retinoids (but not by PGs); 3) The gastric mucosal protection induced by retinoids and gastric mucosal permeability can be separated in time. The existence of gastric mucosal protection can be demonstrated in healthy persons (against indomethacin treatment), in patients with gastric ulcer (GU) and duodenal ulcer (DU) without any inhibition of gastric acid secretion. The serum levels of vitamin A and zeaxanthin were significantly decreased in patients with chronic gastrointestinal (GI) inflammatory diseases (e.g., terminal ileitis, ulcerative colitis), colorectal polyposis, and different (e.g., esophageal, gastric, pancreatic, hepatocellular and colorectal) malignant diseases. The serum levels of vitamin A provitamins were unchanged and their GI mucosal protective effects do not depend on vitamin A activity. Conclusions: 1) Abundant experimental and human observations clearly proved the defensive role of retinoids in the GI tract; 2) There is a correlation between the a) scavenger properties of retinoids vs. intact vagal nerve; b) scavenging properties vs. intact adrenals. 3) The GI mucosal protective effect of retinoids is correlated with biochemical changes in the GI mucosa.

KW - ADP

KW - ATP

KW - cAMP

KW - Gastric mucosal damage

KW - Gastric mucosal protection

KW - Human

KW - Retinoids

UR - http://www.scopus.com/inward/record.url?scp=0035834280&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035834280&partnerID=8YFLogxK

U2 - 10.1016/S0024-3205(01)01416-3

DO - 10.1016/S0024-3205(01)01416-3

M3 - Article

C2 - 11758835

AN - SCOPUS:0035834280

VL - 69

SP - 3103

EP - 3112

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 25-26

ER -