NEUROTOXICITY AND INDUCTION OF FIBROBLAST PROLIFERATION BY ACETALDEHYDE IN THE RABBIT LIVER

• Type: Article in International Scientific Journal
• Date: 1993

Authors

matias, a (Author) FMUP; soares-da-silva, p (Author) FMUP; AZEVEDO, I (Author) Other

Journal

Title: Journal of Autonomic Pharmacology

Vol. 13

Pages: 275-280

ISSN: 0144-1795

Publisher: Blackwell

Indexing

ISI Web of Knowledge - 1 Citation

Scopus - 2 Citations

Other information

Authenticus ID: P-001-MTM

DOI: 10.1111/j.1474-8673.1993.tb00275.x

Abstract (EN): 1 Acetaldehyde may, directly or through the formation of condensation products with biogenic amines, be involved in the pathogeny of alcoholic disease. 2 Rabbits were treated acutely (200 mg kg-1, i.p., 1 h before sacrifice) or subacutely (200 mg kg-1 per day, during 5 days; sacrificed 2 days after end of treatment) with acetaldehyde. Another group was administered 6-OHDA (2 x 50 mg kg-1 on day 0 and on day 1, killed on day 5). 3 Acetaldehyde induced a depletion of hepatic noradrenaline. Both in the acute experiments and 2 days after the subacute treatment with acetaldehyde the levels of hepatic noradrenaline were 25% of control. These effects were similar to, but less intense than those induced by 6-OHDA. 4 Both subacute acetaldehyde and 6-OHDA led to a significant increase in the density of fibroblasts in the portal tract spaces of the rabbit liver. 5 The neurotoxic effects of acetaldehyde and the subsequent increase in liver fibroblast density may play a role in the pathogenesis of alcoholic disease.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 6