Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1998-8-20
|
| pubmed:abstractText |
Livers of fasted rats were perfused over 120 min in a recirculating hemoglobin-free system. Hepatotoxic injury induced by the addition of 1-butanol (130.2 mmol/l), CdCl2 (0.1 mmol/l), CuCl2 (0.03 mmol/l), Na3VO4 (2 mmol/l) or t-butylhydroperoxide (t-BuOOH, 0.5 mmol/l) to the perfusate was shown by strong increases in lactate dehydrogenase (LDH) and glutamate-pyruvate transaminase (GPT) release, decreased oxygen consumption between 50 and 60%, and a nearly complete suppression of bile flow. Hepatic adenosine triphosphate (ATP) and reduced glutathione (GSH) concentrations were reduced by between 30 and 80%, and 20 and 80% respectively. Only Na3VO4 and t-BuOOH evoked increased releases of glutamate dehydrogenase (GLDH) in the perfusate. Malondialdehyde (MDA) concentrations were enhanced by all toxicants in the perfusate and by all except 1-butanol in the liver. The MDA increase, however, was much higher after Na3VO4 and t-BuOOH than after the other toxicants. When glycine (12 mmol/l) was added 30 min before the toxicants to the perfusate it prevented the enzyme releases induced by all hepatotoxic agents by about 80%. Furthermore, glycine prevented the Na3VO4 induced increase of MDA in liver and perfusate, the hepatic ATP and GSH level reductions induced by 1-butanol and attenuated the reduction of oxygen consumption induced by CuCl2 and t-BuOOH. Glycine, however, did not reverse the reductions of oxygen consumption induced by CdCl2 and Na3VO4, the suppressions of bile flow and, with the exception of 1-butanol, the decreases of hepatic ATP levels induced by all agents.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-Butanol,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Alanine Transaminase,
http://linkedlifedata.com/resource/pubmed/chemical/Cadmium,
http://linkedlifedata.com/resource/pubmed/chemical/Copper,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Glycine,
http://linkedlifedata.com/resource/pubmed/chemical/L-Lactate Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Malondialdehyde,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxides,
http://linkedlifedata.com/resource/pubmed/chemical/Vanadates,
http://linkedlifedata.com/resource/pubmed/chemical/tert-Butylhydroperoxide
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0300-483X
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
26
|
| pubmed:volume |
128
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
63-72
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:9704906-1-Butanol,
pubmed-meshheading:9704906-Adenosine Triphosphate,
pubmed-meshheading:9704906-Alanine Transaminase,
pubmed-meshheading:9704906-Animals,
pubmed-meshheading:9704906-Bile,
pubmed-meshheading:9704906-Cadmium,
pubmed-meshheading:9704906-Copper,
pubmed-meshheading:9704906-Drug-Induced Liver Injury,
pubmed-meshheading:9704906-Glutathione,
pubmed-meshheading:9704906-Glycine,
pubmed-meshheading:9704906-L-Lactate Dehydrogenase,
pubmed-meshheading:9704906-Liver,
pubmed-meshheading:9704906-Male,
pubmed-meshheading:9704906-Malondialdehyde,
pubmed-meshheading:9704906-Oxygen Consumption,
pubmed-meshheading:9704906-Perfusion,
pubmed-meshheading:9704906-Peroxides,
pubmed-meshheading:9704906-Rats,
pubmed-meshheading:9704906-Rats, Wistar,
pubmed-meshheading:9704906-Vanadates,
pubmed-meshheading:9704906-tert-Butylhydroperoxide
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Influence of glycine on the damage induced in isolated perfused rat liver by five hepatotoxic agents.
|
| pubmed:affiliation |
Institut für Toxikologie der Medizinischen Universität zu Lübeck, Germany.
|
| pubmed:publicationType |
Journal Article
|