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Vitamin A deficiency alters the bioelectric parameters and RNA content of rat gastric mucosa in vitro

100%

Ventura U., Ceriani T., Montini E., Romano M., Ricci V.

Journal of Physiology and Pharmacology

2003

tom 54

nr 4

The present study was aimed to investigate the mechanisms by which vitamin A plays a role in maintaining the efficiency of gastric mucosal barrier. Particularly, we measured electrical parameters and the RNA/DNA ratio of gastric mucosa isolated in vitro from the stomach of rats in which vitamin A-deficiency was induced by means of a vitamin A-free diet and then abolished by means of a massive vitamin A supplementation. Pair-fed vitamin A-nondepleted rats and normal rats fed ad libitum on a standard diet served as controls. Vitamin A status was assayed for each group of rats by measuring the hepatic content of vitamin A. We found that in gastric mucosa vitamin A-deficiency induced: 1) a decrease in both transmucosal potential difference and short-circuit current; 2) an increase in transmucosal electrical resistance; 3) a decrease in RNA content resulting in a decreased RNA/DNA ratio. Abolishment of vitamin A-deficiency restored both electrical parameters and RNA content of rat gastric mucosa. Our results stress the role of vitamin A in maintaining the efficiency of the gastric mucosal barrier. Vitamin A seems to act by stabilizing gastric electrical parameters and by controlling the protein synthesis/turnover in the surface gastric mucosal cells.

Relationship between Vac A toxin and ammonia in Helicobacter pylori-induced apoptosis in human gastric epithelial cells

72%

Chiozzi V., Mazzini G., Oldani A., Sciullo A., Ventura U., Romano M., Boquet P., Ricci V.

Journal of Physiology and Pharmacology

2009

tom 60

nr 3

23-30

VacA toxin is one of the most important virulence factors produced by H. pylori even though neither its role nor its action mechanisms are completely understood. First considered as a toxin inducing only cell vacuolation, VacA causes apoptosis of gastric epithelial cells by targeting mitochondria. A hotly debated question about VacA action is its relationship with ammonia, which is produced in vivo by H. pylori urease. While ammonia is strictly required for VacA-dependent vacuolation, its role in VacA-induced apoptosis is much less defined. This study was thus aimed to investigate the relationship between VacA toxin and ammonia in H. pylori-induced mitochondrial damage and apoptosis of human gastric epithelial cells in culture by means of flow cytometry. Our results show that, unlike cell vacuolation, in MKN 28 cells neither apoptosis nor dissipation of mitochondrial transmembrane potential induced by VacA require ammonia. Nevertheless, ammonia significantly potentiates both these VacA-induced effects, but independently of the swelling of VacA-containing endosomes (i.e., vacuolation). Our findings make unlikely the hypothesis that ammonia-dependent swelling and rupture of endosomal vesicles in which VacA is sequestered after cell internalization may allow the toxin to reach mitochondria and trigger apoptosis.

Ograniczanie wyników

2 Journal of Physiology and Pharmacology

2 Ricci V.

2 Romano M.

2 Ventura U.

1 Boquet P.

1 Ceriani T.

1 Chiozzi V.

1 Mazzini G.

1 Montini E.

1 Oldani A.

1 Sciullo A.

1 2009

1 2003

Wyniki wyszukiwania

Vitamin A deficiency alters the bioelectric parameters and RNA content of rat gastric mucosa in vitro

Relationship between Vac A toxin and ammonia in Helicobacter pylori-induced apoptosis in human gastric epithelial cells