Free Radical Scavenging and Antioxidative Properties of ‘Silibin’ Complexes on Microsomal Lipid Peroxidation
Article first published online: 4 DEC 1998
Copyright © 1997 John Wiley & Sons, Ltd.
Cell Biochemistry and Function
Volume 15, Issue 1, pages 27–33, March 1997
How to Cite
BASAGA, H., POLI, G., TEKKAYA, C. and ARAS, I. (1997), Free Radical Scavenging and Antioxidative Properties of ‘Silibin’ Complexes on Microsomal Lipid Peroxidation. Cell Biochem. Funct., 15: 27–33. doi: 10.1002/(SICI)1099-0844(199703)15:1<27::AID-CBF714>3.0.CO;2-W
- Issue published online: 4 DEC 1998
- Article first published online: 4 DEC 1998
- Manuscript Accepted: 2 SEP 1996
- Manuscript Received: 15 JUL 1996
- Turkish Science and Research Council. Grant Number: TBGAG-95
- Treaty of collaboration by the Middle East Technical University and the University of Torino
- lipid oxidation;
- free radicals;
The antioxidant properties of silibin complexes, the water-soluble form silibin dihemisuccinate (SDH), and the lipid-soluble form, silibin phosphatidylcholine complex known as IdB 1016, were evaluated by studying their abilities to react with the superoxide radical anion (O2.−), and the hydroxyl radical (OH.). In addition, their effect on pulmonary and hepatic microsomal lipid peroxidation had been investigated. Superoxide radicals were generated by the PMS-NADH system and measured by their ability to reduce NBT. IC50 concentrations for the inhibition of the NBT reduction by SDH and IdB 1016 were found to be 25 μM and 316 μM respectively. Both silibin complexes had an inhibitory effect on xanthine oxidase activity. SDH reacted rapidly with OH. radicals at approximately diffusion controlled rate and the rate constant was found to be (K=8·2×109M−1 s−1); it appeared to chelate Fe2+ in solution.
In hepatic microsomes, when lipid peroxidation was induced by Fe2+, SDH inhibited by 39·5 per cent and IdB 1016 by 19·5 per cent, whereas when lipid peroxidation was induced by CuOOH, IdB 1016 exerted a better protective effect than SDH (29·4 per cent and 19·4 per cent inhibition, respectively). In both microsomal systems lipid peroxidation proceeded through a thiol depletion mechanism which could be restored in the presence of silibin complexes. Low levels of lipid peroxidation in pulmonary microsomes point out the differences between in-vitro lipid peroxidation occurring in microsomes of different tissues.
The results support the free radical scavenger and antioxidative properties of silibin when it is complexed with a suitable molecule to increase its bioavailabilty. © 1997 John Wiley & Sons, Ltd.