Basaga H, Poli G, Tekkaya C, Aras I
Department of Food Engineering, Middle East Technical University, Ankara, Turkey.
Cell Biochem Funct. 1997 Mar;15(1):27-33. doi: 10.1002/(SICI)1099-0844(199703)15:1<27::AID-CBF714>3.0.CO;2-W.
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 microM and 316 microM 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 x 10(9) M-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 bioavailability.
通过研究水飞蓟宾复合物、水溶性形式的水飞蓟宾二半琥珀酸酯（SDH）和脂溶性形式的水飞蓟宾磷脂酰胆碱复合物（称为IdB 1016）与超氧阴离子自由基（O2-.）和羟基自由基（OH.）反应的能力，评估了它们的抗氧化特性。此外，还研究了它们对肺和肝微粒体脂质过氧化的影响。超氧自由基由PMS-NADH系统产生，并通过其还原NBT的能力进行测定。发现SDH和IdB 1016抑制NBT还原的IC50浓度分别为25 microM和316 microM。两种水飞蓟宾复合物均对黄嘌呤氧化酶活性有抑制作用。SDH以近似扩散控制速率与OH自由基快速反应，速率常数为（K = 8.2 x 10(9) M-1 s-1）；它似乎能螯合溶液中的Fe2+。在肝微粒体中，当由Fe2+诱导脂质过氧化时，SDH的抑制率为39.5%，IdB 1016为19.5%，而当由CuOOH诱导脂质过氧化时，IdB 1016的保护作用优于SDH（分别为29.4%和19.4%的抑制率）。在两个微粒体系统中，脂质过氧化均通过硫醇消耗机制进行，在水飞蓟宾复合物存在时该机制可恢复。肺微粒体中低水平的脂质过氧化指出了不同组织微粒体中发生的体外脂质过氧化之间的差异。结果支持了水飞蓟宾与合适分子复合以提高其生物利用度时的自由基清除剂和抗氧化特性。
