N-acetyl cysteine is an early but also a late preventive agent against carbon tetrachloride-induced liver necrosis.
N-Acetyl cysteine (NAC) treatment 30 min before or 6 or 10 h after carbon tetrachloride (CCl4) administration significantly prevented the liver necrosis produced by the hepatotoxin at 24 h. NAC pretreatment was able to partially decrease the covalent binding of CCl4 reactive metabolites at 1 and 3 h of poisoning and, to a small extent, the concentration of CCl4 reaching the liver at 3 h. NAC also diminished partially the CCl4-promoted increases in lipid peroxidation at 3 h, but had an enhancing effect of its own of small intensity. Results suggest that early and late protective effects of NAC might be attributable to its prior conversion to cysteine and glutathione.
Valles
E G
EG
Centro de Investigaciones Toxicológicas (CEITOX) CITEFA/CONICET Zufriategui 4380, Buenos Aires, Argentina.
de Castro
C R
CR
Castro
J A
JA
D000111:Acetylcysteine / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D002251:Carbon Tetrachloride / Q000378:metabolism / Q000633:toxicity*; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000378:metabolism; D009336:Necrosis / Q000139:chemically induced / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley
D002251:Carbon Tetrachloride; D000111:Acetylcysteine