Pietrangelo A, Borella F, Casalgrandi G, Montosi G, Ceccarelli D, Gallesi D, Giovannini F, Gasparetto A, Masini A
Dipartimento di Medicina Interna, University of Modena, Italy.
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.
Rats were fed a 2.5% carbonyl-iron diet and 100 mg.kg body wt-1.day-1 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.
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.
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.
肝脏铁毒性可能由自由基和生物膜的脂质过氧化介导。在实验性铁过载期间，对天然黄酮类化合物的主要成分水飞蓟宾的抗氧化特性进行了体内研究。
给大鼠喂食含2.5%羰基铁的饮食，并给予100mg·kg体重-1·天-1的水飞蓟宾，持续4个月，通过免疫细胞化学、线粒体能量依赖性功能和线粒体丙二醛含量检测肝脏脂质过氧化副产物的积累情况。
铁过载导致丙二醛-蛋白质加合物在充满铁的门周肝细胞中大量积累，而水飞蓟宾处理可明显减少这种积累。水飞蓟宾对铁诱导的线粒体丙二醛积累也有同样的有益作用。关于肝脏功能效率，水飞蓟宾成功抵消了铁过载引起的线粒体能量浪费和组织三磷酸腺苷消耗。
口服水飞蓟宾可在体内预防铁诱导的肝脏毒性。这种作用似乎是由该化合物突出的抗氧化活性引起的。
