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Silybin Dihemisuccinate Protects Against Glutathione Depletion and Lipid Peroxidation Induced by Acetaminophen on Rat Liver
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1989
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Nutraceutical IngredientLipid PeroxidationLipid Peroxidation InducedRedox BiologyOxidative StressToxicologyHepatotoxicityCellular NecrosisBiochemistryLiver PhysiologyMetabolomicsExperimental ToxicologyPharmacologyDrug-induced Liver InjuryRat LiverAcetaminophen HepatotoxicitySilybin DihemisuccinateMetabolismMedicine
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.