Antioxidant activity of silybin in vivo during long-term iron overload in rats

Gastroenterology. 1995 Dec;109(6):1941-9. doi: 10.1016/0016-5085(95)90762-9.


Background & aims: Hepatic iron toxicity may be mediated by free radical species and lipid peroxidation of biological membranes. The antioxidant property of silybin, a main constituent of natural flavonoids, was investigated in vivo during experimental iron overload.

Methods: Rats were fed a 2.5% carbonyl-iron diet and 100 body silybin for 4 months and were assayed for accumulation of hepatic lipid peroxidation by-products by immunocytochemistry, mitochondrial energy-dependent functions, and mitochondrial malondialdehyde content.

Results: Iron overload caused a dramatic accumulation of malondialdehyde-protein adducts into iron-filled periportal hepatocytes that was decreased appreciably by silybin treatment. The same beneficial effect of silybin was found on the iron-induced accumulation of malondialdehyde in mitochondria. As to the liver functional efficiency, mitochondrial energy wasting and tissue adenosine triphosphate depletion induced by iron overload were successfully counteracted by silybin.

Conclusions: Oral administration of silybin protects against iron-induced hepatic toxicity in vivo. This effect seems to be caused by the prominent antioxidant activity of this compound.

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Antioxidants / pharmacology*
  • Chemical and Drug Induced Liver Injury
  • Energy Metabolism
  • Female
  • Glutathione / metabolism
  • Hemosiderosis / prevention & control*
  • Immunohistochemistry
  • Iron / metabolism
  • Lipid Peroxidation / drug effects
  • Liver / drug effects
  • Liver / metabolism
  • Liver Diseases / metabolism
  • Liver Diseases / prevention & control
  • Male
  • Malondialdehyde / metabolism
  • Mitochondria, Liver / drug effects
  • Mitochondria, Liver / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Silymarin / pharmacology*


  • Antioxidants
  • Silymarin
  • Malondialdehyde
  • Adenosine Triphosphate
  • Iron
  • Glutathione