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Effect of different chemicals on thioacetamine-induced liver necrosis.

Abstract：

:Several inhibitors of cytochrome P-450 mediated oxidative transformations, ethyl 2-diethylaminoethyl-2-phenyl-2-ethylmalonate, ethyl-2-diethyl-aminoethyl-2-ethyl-2-buthylmalonate, 2,4 dichloro-6-phenoxyethyl diethylamine, 2-diethylaminoethyl-2-phenyl- (2-propene)-4-penten-1-oate or 3-amino,1,2,4 triazole were not able to significantly prevent thiocetamide induced necrosis at 24 h as evidenced by isocitric acid dehydrogenase activity or histologically. In contrast, several other sulfur containing compounds, tetraethyl thiuramidisulfide, diethyldithiocarbamic acid, thiourea or 1-methyl-2-mercaptoimidazole, which are inhibitors of non-cytochrome P-450 dependent amine oxidase systems, significantly prevented thioacetamide induced liver necrosis at 24 h. Notwithstanding, diphenhydramine, nicotinamide, trimethylamine and imipramine, which are substrates of this amino oxidase system, do not protect. All the chemicals tested prolonged the pentobarbital sleeping time, but there is no correlation between the intensity of this effect and their ability for preventing thioacetamide liver necrosis. These observations suggest that cytochrome P-450 does not play a major role in the activation of thioacetamide to a proximal or an ultimate necrogenic metabolite. Other microsomal enzymes metabolizing sulfur compounds could be involved in the major activation process.

journal_name

Toxicology

journal_title

Toxicology

authors

de Ferreyra EC,de Fenos OM,Castro JA

doi

10.1016/0300-483x(80)90117-1

subject

Has Abstract

pub_date

1980-01-01 00:00:00

pages

205-14

issue

3

eissn

0300-483X

issn

1879-3185

pii

0300-483X(80)90117-1

journal_volume

16

pub_type

杂志文章

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