PROTECTION BY ASCORBIC-ACID AGAINST OXIDATIVE INJURY OF ISOLATED HEPATOCYTES

Citation
E. Maellaro et al., PROTECTION BY ASCORBIC-ACID AGAINST OXIDATIVE INJURY OF ISOLATED HEPATOCYTES, Xenobiotica, 24(3), 1994, pp. 281-289
Citations number
32
Categorie Soggetti
Pharmacology & Pharmacy
Journal title
ISSN journal
00498254
Volume
24
Issue
3
Year of publication
1994
Pages
281 - 289
Database
ISI
SICI code
0049-8254(1994)24:3<281:PBAAOI>2.0.ZU;2-K
Abstract
1. The ability of ascorbic acid to protect from prooxidant-induced tox ic injury was investigated in isolated, intact rat hepatocytes, whose ascorbic acid content had been restored by means of exogenous suppleme ntation. 2. Ascorbate-supplemented and ascorbate-non-supplemented cell s in suspension were treated with a series of different prooxidants (a llyl alcohol, diethyl maleate, carbon tetrachloride, menadione), and t he development of lipid peroxidation and cell injury was evaluated. 3. With allyl alcohol and diethyl maleate, ascorbic acid was able to pro tect cells from both lipid peroxidation and cell injury. The same prot ection was offered by ascorbate also in hepatocytes obtained from vita min E-deficient animals. 4. With carbon tetrachloride, ascorbate suppl ementation did not affect the initial steps of lipid peroxidation, but nevertheless provided a marked protection against lipid peroxidation and cell injury at later times of incubation. The protection was unaff ected by the vitamin E content of cells. 5. With menadione, a toxin wh ich does not induce lipid peroxidation, ascorbic acid did not protect cells against injury. 6. It is concluded that ascorbic acid can act as an efficient antioxidant in isolated rat liver cells, with protection against cell injury. The antioxidant effect appears primarily to invo lve membrane lipids, and can be independent from the cellular content of vitamin E, thus suggesting that ascorbic acid can play a direct and independent role in the intact cell, in addition to its synergistic i nteraction with vitamin E described in other models.