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PubMed1986

Molecular aspects of cytoprotection by modified somatostatins.

Somatostatin and cyclic modifications of this molecule inhibit the development of protrusions on the surface of isolated hepatocytes in presence of phalloidin. This prevention of phalloidin injury is caused by competitive inhibition of the phallotoxin uptake. Transport inhibition is not a hormonal effect of somatostatin. The concentrations needed are in the micromolar range. The most protective somatostatin modifications lack hormonal activity (GH release). Somatostatin and its analogs are substrates of a hepatocellular transporter which also translocates other cyclopeptides, among them phalloidin, antamanide, and several organic anions, such as iodipamide and fusidic acid. Physiological substrates of this multispecific transport system are bile acids. The protection of phallotoxin injury by somatostatin is a specific mechanism only representative for liver cells. No other cell contains the above multispecific transporter.

Affinity Labels↗
PubMed1989

Role of sulfhydryls in mucosal injury caused by ethanol: relation to microvascular permeability, gastric motility and cytoprotection.

The relationship between gastric mucosal glutathione (GSH) levels, vascular permeability, gastric motility and mucosal injury caused by ethanol was investigated in rats. Oral administration of 50% ethanol (1 ml) produced elongated reddish bands of lesions in the mucosa with a significant reduction of GSH levels and increase of microvascular permeability. These lesions were significantly inhibited by pretreatment with s.c. administered diethylmaleate (DEM: 1 ml/kg), cysteamine (100 mg/kg) and 16, 16-dimethyl prostaglandin E2 (dmPGE2, 10 micrograms/kg) but worsened markedly by N-ethylmaleimide (NEM: 10 mg/kg). Irrespective of whether the animals were treated with 50% ethanol or not, the mucosal GSH levels were significantly decreased or increased, respectively, by DEM or cysteamine, and were not affected by both NEM and dmPGE2. NEM significantly enhanced the vascular permeability in the absence or presence of ethanol (greater than 10%), whereas other agents significantly inhibited only the increased vascular permeability caused by ethanol. On the other hand, gastric motility was potently and persistently inhibited by either DEM, cysteamine or dmPGE2 at the doses which prevented ethanol-induced mucosal injury, whereas NEM had no effect on the motility. These results suggest that 1) the mucosal GSH levels do not relate directly to either development or prevention of ethanol-induced gastric injury, 2) potentiation by NEM of the mucosal injury may be accounted for by its enhancement of the vascular permeability and 3) inhibition of gastric motility may be associated with prevention of mucosal lesions.

16,16-Dimethylprostaglandin E2↗
PubMed1986

Cytoprotective effect of free radical scavengers against mucosal damage produced by different antirheumatic drugs.

Following 200 mg aspirin, 20 mg indomethacin or 100 mg diclofenac, gastric mucosal damage was evoked after five hours in rats. By administering vitamin A, vitamin E, MTDQ (6,6-methylenebis-2,2,4-trimethyl-1,2-dihydroquinoline), vitamin C, lipoic acid and penicillamine intragastrically at the time of the application of the damaging agent, the authors studied the beneficial effect of these free-radical scavengers upon the mucosal lesions. Vitamin C and penicillamine exerted no significant protective effect. Among the other drugs, the most effective were the lipid-soluble ones: vitamin A, vitamin E and MTDQ. The authors hypothesized that the gastric damage may be connected with the degradation of the polyunsaturated fatty acid components of the cellular membranes and thus the lipid-soluble free radical scavengers were able to offer protection.

Animals↗