Lipid peroxidation and covalent binding in the early functional impairment of liver Golgi apparatus by carbon tetrachloride.

The onset of the lipoprotein secretory block provoked by CCl4 in the whole animal was monitored after purification of liver Golgi membranes. Both lipid transit through the apparatus and hexosylation of the lipoprotein are markedly inhibited 5-15 min after poisoning. Pre-treating the animal with alpha-tocopherol, shown to prevent lipid peroxidation without modifying the covalent binding due to CCl4 metabolites, affords little protection against lipid accumulation in the Golgi, but total preservation of galactosyl transferase activity. While haloalkylation therefore appears to be the major mechanism of damage in the early phases of CCl4-induced derangement of lipid secretion, lipid peroxidation is probably more involved later; this is indicated by the marked, though never complete, protection against fatty liver afforded at 24 h after CCl4 poisoning by supplementation of the membrane with alpha-tocopherol.
AuthorsG Poli, D Cottalasso, M A Pronzato, E Chiarpotto, F Biasi, F P Corongiu, U M Marinari, G Nanni, M U Dianzani
JournalCell biochemistry and function (Cell Biochem Funct) Vol. 8 Issue 1 Pg. 1-10 (Jan 1990) ISSN: 0263-6484 [Print] ENGLAND
PMID2111233 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Lipids
  • Palmitates
  • Triglycerides
  • Vitamin E
  • Galactosyltransferases
  • Animals
  • Carbon Tetrachloride Poisoning (metabolism)
  • Cell Fractionation
  • Galactosyltransferases (metabolism)
  • Glycosylation
  • Golgi Apparatus (drug effects, metabolism)
  • Lipid Peroxidation (drug effects)
  • Lipids (secretion)
  • Liver (drug effects, metabolism)
  • Male
  • Microsomes, Liver (metabolism)
  • Palmitates (metabolism)
  • Rats
  • Rats, Inbred Strains
  • Triglycerides (metabolism)
  • Vitamin E (administration & dosage)

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