COURSE OF ATP DEPLETION IN HYDRAZINE HEPATOTOXICITY

被引：34

作者：

PREECE, NE

GHATINEH, S

TIMBRELL, JA

机构：

[1] Toxicology Unit, School of Pharmacy, University of London, London, WC1N 1AX

来源：

ARCHIVES OF TOXICOLOGY | 1990年 / 64卷 / 01期

基金：

英国惠康基金;

关键词：

!sup]31[!/sup]P-NMR; ATP; Hepatocytes; Hydrazine; Thiopentobarbitone;

D O I：

10.1007/BF01973376

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

The effect of hydrazine on ATP levels has been investigated in rats in vivo and in hepatocytes in vitro. Hydrazine was found to cause a dose-dependent depletion of hepatic ATP in vivo 3 h after dosing. In isolated hepatocytes in vitro hydrazine also caused a concentration-dependent depletion of ATP which preceded cytotoxicity as indicated by loss of cell viability. The ATP depletion in isolated hepatocytes was also significant at a concentration of hydrazine which was not cytotoxic. Attempts to determine hepatic ATP depletion in vivo over time using topical31P NMR were confounded by the effects of the thiopentobarbitone used to anaesthetise the animals. This was found to ameliorate the effects of hydrazine on ATP depletion but potentiate the lethality of hydrazine. Consequently, although ATP depletion was detected in some hydrazine-treated animals, this was only observed in animals which subsequently died. The results indicate that ATP depletion may underlie the hepatotoxicity of hydrazine. © 1990 Springer-Verlag.

引用

页码：49 / 53

页数：5

共 35 条

[1] OBSERVATION OF H-1-NMR SIGNALS WITH RECEIVER COILS TUNED FOR OTHER NUCLIDES [J].