Silybin dihemisuccinate protects against glutathione depletion and lipid peroxidation induced by acetaminophen on rat liver

Acetaminophen hepatotoxicity is characterized by glutathione depletion, cellular necrosis, and, in some instances, by the induction of lipid peroxidation. Silybin dihemisuccinate, a soluble form of the flavonoid silymarin, protects rats against liver glutathione depletion and lipid peroxidation indu...

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Bibliographic Details
Published inPlanta medica Vol. 55; no. 5; pp. 417 - 419
Main Authors Campos, R, Garrido, A, Guerra, R, Valenzuela, A
Format Journal Article
LanguageEnglish
Published Germany 01.10.1989
Subjects
acetaminophen
Acetaminophen - antagonists & inhibitors
Acetaminophen - pharmacology
Animals
antidotes
flavonoids
Flavonoids - pharmacology
glutathione
Glutathione - metabolism
hepatotoxicity
Lipid Peroxidation - drug effects
liver
Liver - drug effects
Liver - metabolism
Male
Rats
Rats, Inbred Strains
Silybum marianum
silymarin
Silymarin - analogs & derivatives
Silymarin - pharmacology
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Summary:Acetaminophen hepatotoxicity is characterized by glutathione depletion, cellular necrosis, and, in some instances, by the induction of lipid peroxidation. Silybin dihemisuccinate, a soluble form of the flavonoid silymarin, protects rats against liver glutathione depletion and lipid peroxidation induced by acute acetaminophen intoxication. Other biochemical parameters such as serum transaminases did not show the drastic increase observed under acetaminophen intoxication when animals were treated with the flavonoid. Preliminary results suggest that silybin dihemisuccinate may be another antidote against acetaminophen hepatotoxicity.
ISSN:0032-0943
1439-0221
DOI:10.1055/s-2006-962055