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Resistance of the regenerating liver to hepatotoxins

Bulletin of Experimental Biology and Medicine, 1976
Administration of CCl4 and paracetamol to mice causes massive necrosis of the central regions of the hepatic lobule. Preliminary stimulation of hepatocyte proliferation by partial hepatectomy greatly reduces the intensity of the toxic effect or abolishes it completely, depending on the time elapsing after the operation.
I. V. Uryvaeva, V. M. Faktor
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OXIDATIVE BIOACTIVATION OF HALOFORMS INTO HEPATOTOXINS

1980
This chapter discusses the oxidative bioactivation of haloforms into hepatotoxins. The hepatotoxin chloroform (CHCl 3 ) is converted to phosgene (COCl 2 ) by rat liver microsomes and in living rats. The reaction is oxygen dependent and appears to be catalyzed by cytochrome P-450.
L.R. Pohl   +3 more
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Hepatotoxin-induced hypertaurinuria: a proton NMR study

Archives of Toxicology, 1990
The urinary excretion of taurine by rats after dosing with various hepatotoxins has been investigated by 1H NMR spectroscopy. After single hepatotoxic doses of hydrazine, carbon tetrachloride, 1-naphthylisothiocyanate, or thioacetamide there was biochemical and histopathological evidence of hepatic damage. Proton NMR spectroscopy of the urine collected
S M, Sanins   +3 more
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Effect of hyperoxia on liver necrosis induced by hepatotoxins

Virchows Archiv B Cell Pathology Including Molecular Pathology, 1986
We have tested the effects of hyperbaric oxygen on necrosis of rat liver induced by the administration of several toxins. The extent of liver necrosis was determined 24 h after the administration of the toxins by measurement of serum levels of alanine and aspartate amino-transferases and by histologic and ultrastructural analyses.
L, Marzella, K, Muhvich, R A, Myers
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The effect of some hepatotoxins on the sulphoxidation of cimetidine in rat

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 1986
Sulphoxidation of cimetidine was investigated in male and female rats after pretreatment with the hepatotoxins allyl alcohol, dl-ethionine, thioacetamide and carbon tetrachloride. There was a marked sex difference in cimetidine sulphoxidation in response to the hepatotoxin pretreatment.
P A, Dixon, A U, Udeagha
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Toxicity of hepatotoxins: new insights into mechanisms and therapy

Expert Opinion on Investigational Drugs, 1999
Liver injury caused by hepatotoxins, such as carbon tetrachloride (CCl4), ethanol, and acetaminophen (APAP), is characterised by varying degrees of hepatocyte degeneration and cell death via either apoptosis or necrosis. The generation of reactive intermediate metabolites from the metabolism of hepatotoxins, and the occurrence of reactive oxygen ...
J, Wu, A, Danielsson, M A, Zern
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Disposition of the hepatotoxin α-naphthylisothiocyanate (ANIT) in the rat

Toxicology and Applied Pharmacology, 1970
Abstract The disposition of ANIT was investigated in the rat by examining quantitatively the tissue, organ, and subcellular distribution as well as the excretion pattern, of 14C at selected times after ANIT-14C administration. Approximately 70% of the radioactive material was absorbed from the gastrointestinal tract within 24 hr and was found widely ...
F, Capizzo, R J, Roberts
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[Resistance of regenerating liver to hepatotoxins].

Biulleten' eksperimental'noi biologii i meditsiny, 1976
Treatment of mice with CCl4 and paracetamol induced massive centrilobular necroses. Preliminary induction of hepatocyte proliferation by partial hepatectomy significantly weakened or completely eliminated the toxic action on the liver depending on the time passed after the operation.
I V, Uryvaeva, V M, Faktor
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Hepatotoxins

2020
Anup Ramachandran, Hartmut Jaeschke
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