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Inflammation, an inducer of metallothionein, inhibits carbon-tetrachloride-induced hepatotoxicity in rats.

Abstract
Inflammation, induced by turpentine (0.1 ml i.m.), protected against carbon tetrachloride (CCl4)-induced hepatotoxicity based on serum activities of sorbitol dehydrogenase. Inflammation was confirmed by elevated serum ceruloplasmin activities, and was associated with high hepatic levels of metallothionein, a zinc protein proposed to protect against CCl4-induced injury. Inflammation suppressed cytochrome P-450 activities, but this was not associated with protection against CCl4-promoted liver microsomal injury as assessed by glucose-6-phosphatase activity loss. Thus, protection against plasma membrane injury did not result primarily from depressed microsomal activation of CCl4. Each effect of inflammation reported here resembled effects of zinc injections. This similarity strengthens the hypothesis that metallothionein protects against CCl4-induced hepatic plasma membrane injury.
AuthorsR A DiSilvestro, G P Carlson
JournalToxicology letters (Toxicol Lett) Vol. 60 Issue 2 Pg. 175-81 (Apr 1992) ISSN: 0378-4274 [Print] Netherlands
PMID1315082 (Publication Type: Journal Article)
Chemical References
  • Cytochrome P-450 Enzyme System
  • Metallothionein
  • L-Iditol 2-Dehydrogenase
  • Ceruloplasmin
  • Glucose-6-Phosphatase
  • Turpentine
Topics
  • Animals
  • Carbon Tetrachloride Poisoning (prevention & control)
  • Ceruloplasmin (metabolism)
  • Cytochrome P-450 Enzyme System (metabolism)
  • Glucose-6-Phosphatase (metabolism)
  • Inflammation (chemically induced, metabolism)
  • Injections, Intramuscular
  • L-Iditol 2-Dehydrogenase (blood)
  • Liver (drug effects, metabolism)
  • Male
  • Metallothionein (metabolism)
  • Rats
  • Rats, Inbred Strains
  • Turpentine

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