1. cellular concentrations of reduced glutathione or reduced conjugating ability. Whatever the cause;Mitchell, JR, Jollow; DJ, Potter; WZ, Davies; DC, JR, Gillette; Brodie, B.B.,1973
2. The rise in plasma GST which we observed within 30 minutes of NAC infusion may have been coincidental and caused solely by paracetamol toxicity but the time course of the rise in GST suggests that NAC treatment may itself result in a release of a small amount of GST from the hepatocyte in to plasma. Studies on isolated rat hepatocytes tend to support this view because high concentrations of Gillette JR, Brodie BB. Acetaminophen-induced hepatic necrosis. II. Role of covalent binding in vivo;Jollow, D.J.; Mitchell, JR, Potter; WZ, Davies; D.C.;J Pharmacol Exp Ther,1973
3. Acetaminophen-induced hepatic necrosis. III. Cytochrome P-450-mediated covalent binding in vitro;Potter, W.Z.; Davies, D.C.; Mitchell, JR, Jollow; DJ, JR, Gillette; Brodie, B.B.;J Pharmacol Exp Ther,1973
4. Pharmacol Exp In man clarification of this point by control experiments - that is, NAC infusion in the absence of paracetamol poisoning and no NAC infusion after a paracetamol overdose, in patients requiring treatment and admitted within 8 hours - would be unethical. Comparison of peak GST values found in severe;paracetamol-induced liver damage with peak Ther,1973
5. Treatment of paracetamol (acetaminophen) poisoning with N-acetylcysteine;Prescott, L.F.; Park, J.; Ballantyne, A.; Adriaenssens, P.; Proudfoot, A.T.;Lancet,1977