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[Depletion of liver glutathione induced by iodobenzene poisoning and its relation to lipid peroxidation and necrosis].

Abstract
The mechanisms underlying iodobenzene hepatotoxicity were investigated in Albino mice in which the hepatic glutathione (GSH) content had been decreased by nearly 50% by starvation for 16 h before poisoning. After iodobenzene administration (9 mmol/Kg, p.o.) the hepatic GSH content decreased progressively and liver necrosis, as measured by the plasma transaminase (GPT, GOT) levels, occurred in many animals at 12 and 16 h. A clear cut necrosis was evident only when the hepatic GSH depletion reached a threshold value (3.5-2.5 nmol/mg protein). The same threshold value was evident for the occurrence of lipid peroxidation (measured as both carbonyl functions and conjugated dienes in liver phospholipids). The highly significant correlation found between lipid peroxidation and liver necrosis supports the possibility of a cause-effect relationship between the two phenomena.
AuthorsA F Casini, A Pompella, M Comporti
JournalBollettino della Societa italiana di biologia sperimentale (Boll Soc Ital Biol Sper) Vol. 59 Issue 11 Pg. 1725-31 (Nov 30 1983) ISSN: 0037-8771 [Print] Italy
Vernacular TitleDeplezione di glutatione epatico indotta dall'intossicazione con iodobenzene e suoi rapporii con la perossidazione lipidica e la necrosi.
PMID6667314 (Publication Type: English Abstract, Journal Article)
Chemical References
  • Iodobenzenes
  • Lipid Peroxides
  • iodobenzene
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glutathione
Topics
  • Alanine Transaminase (blood)
  • Animals
  • Aspartate Aminotransferases (blood)
  • Glutathione (metabolism)
  • Iodobenzenes (toxicity)
  • Lipid Peroxides (metabolism)
  • Liver (drug effects, pathology)
  • Mice
  • Necrosis

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