Increased carbon tetrachloride hepatotoxicity after low-level ethanol consumption.

Abstract:

:Male rats provided with a 5 or 15% (v/v) ethanol solution as the sole source of fluid consumed ethanol at a rate of 11.4 or 24.9% of total calories (4.2 or 8.3 g/kg daily). After ethanol consumption lasting 1, 2 and 3 weeks the hepatotoxicity of CCl4 (0.1 ml/kg i.p.) was elevated by determination of serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase ( GPT), sorbitol dehydrogenase (SDH) and histological investigations. Carbon tetrachloride (CCl4)-induced liver damage was significantly greater in rats provided with ethanol than in the tap-water consuming controls. This potentiation of CCl4 hepatotoxicicty was fully developed already after a 1-week exposition to ethanol and was greater in the 15% than in the 5% ethanol group. Ethanol alone did not influence serum enzyme activities but increased microsomal aniline hydroxylation. There was, however, no clear-cut parallelism between potentiation of CCl4 hepatotoxicity and activation of aniline hydroxylation.

journal_name

Toxicology

journal_title

Toxicology

authors

Strubelt O,Obermeier F,Siegers CP,Vöpel M

doi

10.1016/0300-483x(78)90076-8

subject

Has Abstract

pub_date

1978-07-01 00:00:00

pages

261-70

issue

3

eissn

0300-483X

issn

1879-3185

journal_volume

10

pub_type

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