PMID- 10817630
OWN - NLM
STAT- MEDLINE
DCOM- 20000628
LR  - 20190819
IS  - 0378-4274 (Print)
IS  - 0378-4274 (Linking)
VI  - 115
IP  - 1
DP  - 2000 Apr 10
TI  - Prolonged phenobarbital pretreatment abolishes the early oxidative stress 
      component induced in the liver by acute lindane intoxication.
PG  - 45-51
AB  - Lindane administration to rats (60 mg/kg b.w.) led to an enhancement in the 
      oxidative stress status of the liver at 4 h after treatment, characterized by 
      increases in hepatic thiobarbituric acid reactants (TBARS) formation and 
      chemiluminescence, reduced glutathione (GSH) depletion, and diminution in the 
      biliary content and release of GSH. These changes were observed in the absence of 
      changes in either microsomal functions (cytochrome P450 content, NADPH-dependent 
      superoxide radical production, and NADPH-cytochrome P450 reductase or NADPH 
      oxidase activities) or in oxidative stress-related enzymatic activities 
      (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, 
      glucose-6-phosphate dehydrogenase, and glutathione-S-transferases), over control 
      values. Phenobarbital (PB) administration (0.1% in drinking water; 15 days) 
      elicited an enhancement in liver microsomal functions, lipid peroxidation, and 
      GSH content, without changes in oxidative stress-related enzymatic activities, 
      except for the elevation in those of glutathione reductase and 
      glutathione-S-transferase, compared to control rats. Lindane given to 
      PB-pretreated rats did not alter liver microsomal functions, lipid peroxidation, 
      glutathione status, or oxidative stress-related enzymatic activities, as compared 
      to PB-pretreated animals. In addition, lindane induced periportal necrosis with 
      hemorrhagic foci in untreated rats, but not in PB-pretreated animals. It is 
      concluded that the early oxidative stress response of the liver to lindane and 
      hepatic injury are suppressed by PB pretreatment via induction of microsomal 
      enzymes in all zones of the hepatic acinus. reserved.
FAU - Videla, L A
AU  - Videla LA
AD  - Programa de Farmacologia Molecular y Clinica, Instituto de Ciencias Biomedicas, 
      Facultad de Medicina, Universidad de Chile, Santiago.
FAU - Arisi, A C
AU  - Arisi AC
FAU - Fuzaro, A P
AU  - Fuzaro AP
FAU - Koch, O R
AU  - Koch OR
FAU - Junqueira, V B
AU  - Junqueira VB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 59NEE7PCAB (Hexachlorocyclohexane)
RN  - YQE403BP4D (Phenobarbital)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Biotransformation
MH  - Chemical and Drug Induced Liver Injury
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Hexachlorocyclohexane/antagonists & inhibitors/blood/*poisoning
MH  - Lipid Peroxidation/drug effects
MH  - Liver/drug effects
MH  - Liver Diseases/*prevention & control
MH  - Male
MH  - Oxidative Stress/*drug effects
MH  - Phenobarbital/*pharmacology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2000/05/19 09:00
MHDA- 2000/07/06 11:00
CRDT- 2000/05/19 09:00
PHST- 2000/05/19 09:00 [pubmed]
PHST- 2000/07/06 11:00 [medline]
PHST- 2000/05/19 09:00 [entrez]
AID - S0378-4274(00)00172-7 [pii]
AID - 10.1016/s0378-4274(00)00172-7 [doi]
PST - ppublish
SO  - Toxicol Lett. 2000 Apr 10;115(1):45-51. doi: 10.1016/s0378-4274(00)00172-7.