Acetaminophen metabolism by the perfused rat liver twelve hours after acetaminophen overdose
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Acetaminophen metabolism by the perfused rat liver twelve hours after acetaminophen overdose. / Poulsen, Henrik E.; Lerche, Anette; Skovgaard, Lene T.
In: Biochemical Pharmacology, Vol. 34, No. 20, 15.10.1985, p. 3729-3733.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Acetaminophen metabolism by the perfused rat liver twelve hours after acetaminophen overdose
AU - Poulsen, Henrik E.
AU - Lerche, Anette
AU - Skovgaard, Lene T.
PY - 1985/10/15
Y1 - 1985/10/15
N2 - The effect of a toxic dose of acetaminophen on the hepatic conjugations of acetaminophen was studied in single pass perfused livers from rats given acetaminophen overdose 12 hr prior to perfusion and from control rats. Four different acetaminophen concentrations (0.1-6 mmol/1) were used in each perfusion. Glucuronidation of acetaminophen was increased and sulfation of acetaminophen occurred at an unchanged rate in acetaminophen damaged livers as compared to control livers. Hepatic glutathione concentrations declined to about 0.4μmol/g liver during perfusion, possibly due to excretion of glutathione to perfusion medium, but in spite of this the formation of glutathione conjugates was increased with acetaminophen concentrations increasing up to about 5 mmol. We conclude that decreased sulfation, glucuronidation and glutathione conjugation in the liver is not present in the early development of acetaminophen-induced hepatic damage.
AB - The effect of a toxic dose of acetaminophen on the hepatic conjugations of acetaminophen was studied in single pass perfused livers from rats given acetaminophen overdose 12 hr prior to perfusion and from control rats. Four different acetaminophen concentrations (0.1-6 mmol/1) were used in each perfusion. Glucuronidation of acetaminophen was increased and sulfation of acetaminophen occurred at an unchanged rate in acetaminophen damaged livers as compared to control livers. Hepatic glutathione concentrations declined to about 0.4μmol/g liver during perfusion, possibly due to excretion of glutathione to perfusion medium, but in spite of this the formation of glutathione conjugates was increased with acetaminophen concentrations increasing up to about 5 mmol. We conclude that decreased sulfation, glucuronidation and glutathione conjugation in the liver is not present in the early development of acetaminophen-induced hepatic damage.
UR - http://www.scopus.com/inward/record.url?scp=0022229944&partnerID=8YFLogxK
U2 - 10.1016/0006-2952(85)90238-2
DO - 10.1016/0006-2952(85)90238-2
M3 - Journal article
C2 - 4052111
AN - SCOPUS:0022229944
VL - 34
SP - 3729
EP - 3733
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
SN - 0006-2952
IS - 20
ER -
ID: 259167585