Dresow B, Albert C, Zimmermann I, Nielsen P
Abteilung Medizinische Biochemie, Physiologisch-Chemisches Institut, Universitätskrankenhaus, Hamburg, Germany.
Hepatology. 1995 Apr;21(4):1099-105.
Organ damage caused by iron overload has been mostly attributed to iron-induced peroxidation of membrane lipids. Using the ferrocene iron-loaded rat model, we studied ethane exhalation as a direct marker of in vivo lipid peroxidation, as well as concentrations of alpha-tocopherol and ubiquinol 9/10 in liver and plasma as indirect markers of this process. The feeding of a diet enriched with 0.5% TMH-ferrocene up to 31 weeks resulted in a large increase in liver iron concentration to about 25 mg/g wet weight (w wt). At lower, predominantly hepatocellular liver siderosis, the breath ethane exhalation was dependent on dietary vitamin E (VitE) supplements (onset of ethane exhalation at liver-Fe > 2 mg/g w wt on vitE-restricted diet; > 5 mg Fe per gram on VitE-replete diet). At severe liver siderosis, breath ethane exhalation reached a maximum of approximately 8 nmol/kg/hr independent of VitE supplementation. Plasma as well as hepatic alpha-tocopherol decreased with progressive iron loading. In addition, a significant depletion in hepatic ubiquinol 9 and 10 was noted.
铁过载引起的器官损伤主要归因于铁诱导的膜脂质过氧化。我们使用二茂铁铁负载大鼠模型，研究了乙烷呼出量作为体内脂质过氧化的直接标志物，以及肝脏和血浆中α-生育酚和泛醇9/10的浓度作为该过程的间接标志物。喂食富含0.5%TMH-二茂铁的饮食长达31周，导致肝脏铁浓度大幅增加至约25mg/g湿重（w wt）。在较低程度、主要为肝细胞性肝铁沉着症时，呼出的乙烷量取决于膳食维生素E（VitE）补充剂（在维生素E限制饮食中，肝脏铁含量>2mg/g w wt时开始呼出乙烷；在维生素E充足饮食中，每克铁含量>5mg时开始呼出乙烷）。在严重肝铁沉着症时，呼出的乙烷量最高可达约8nmol/kg/小时，与是否补充维生素E无关。随着铁负荷的增加，血浆和肝脏中的α-生育酚含量均下降。此外，还发现肝脏中的泛醇9和10显著减少。
