PMID- 27415022
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160716
LR  - 20160715
IS  - 1351-0002 (Print)
IS  - 1351-0002 (Linking)
VI  - 3
IP  - 4
DP  - 1997 Aug
TI  - Acetaminophen-induced liver oxidative stress and hepatotoxicity: influence of 
      Kupffer cell activity assessed in the isolated perfused rat liver.
PG  - 213-8
LID - 10.1080/13510002.1997.11747112 [doi]
AB  - The influence of acetaminophen (APAP) treatment (400 mg/kg) on Kupffer cell 
      function was studied in the isolated perfused liver by colloidal carbon infusion, 
      concomitantly with parameters related to oxidative stress (thiobarbituric acid 
      reactants (TBARS) formation and glutathione (GSH) content) and tissue injury 
      (sinusoidal efflux of lactate dehydrogenase (LDH)). APAP led to increased rates 
      of hepatic TBARS formation, GSH depletion, and higher sinusoidal LDH efflux 
      compared to control values, without changes in the basal rate of O2 consumption. 
      In addition, APAP significantly enhanced the rate of carbon uptake by perfused 
      livers and the associated carbon-induced O2 consumption, with carbon-induced LDH 
      effluxes being increased by 411% over control values or by 124% compared to basal 
      LDH release in APAP-treated rats. APAP-induced changes in liver TBARS formation 
      and GSH levels were attenuated by gadolinium chloride (GdCl3) pretreatment, 
      whereas those in carbon uptake, carbon-induced respiration, and LDH efflux were 
      abolished. GdCl3 pretreatment decreased liver O2 consumption irrespectively of 
      APAP treatment, an effect that seems to be due to depression of mitochondrial 
      respiration. It is concluded that APAP intoxication enhances Kupffer cell 
      function as assessed in the intact liver, which may represent an important source 
      of reactive O2 species and chemical mediators conditioning the increased 
      oxidative stress status and the tissue injury which developed.
FAU - Tapia, G
AU  - Tapia G
AD  - a Programa de Farmacologia Molecular y Clinica , Instituto de Ciencias Biomedicas 
      , Facultad de Medicina , Universidad de Chile , Santiago , Chile.
FAU - Cornejo, P
AU  - Cornejo P
AD  - a Programa de Farmacologia Molecular y Clinica , Instituto de Ciencias Biomedicas 
      , Facultad de Medicina , Universidad de Chile , Santiago , Chile.
FAU - Ferreira, J
AU  - Ferreira J
AD  - a Programa de Farmacologia Molecular y Clinica , Instituto de Ciencias Biomedicas 
      , Facultad de Medicina , Universidad de Chile , Santiago , Chile.
FAU - Fernandez, V
AU  - Fernandez V
AD  - a Programa de Farmacologia Molecular y Clinica , Instituto de Ciencias Biomedicas 
      , Facultad de Medicina , Universidad de Chile , Santiago , Chile.
FAU - Videla, L A
AU  - Videla LA
AD  - a Programa de Farmacologia Molecular y Clinica , Instituto de Ciencias Biomedicas 
      , Facultad de Medicina , Universidad de Chile , Santiago , Chile.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Redox Rep
JT  - Redox report : communications in free radical research
JID - 9511366
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 2016/07/15 06:00
PHST- 2016/07/15 06:00 [entrez]
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
AID - 10.1080/13510002.1997.11747112 [doi]
PST - ppublish
SO  - Redox Rep. 1997 Aug;3(4):213-8. doi: 10.1080/13510002.1997.11747112.