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Ethane exhalation and vitamin E/ubiquinol status as markers of lipid peroxidation in ferrocene iron—loaded rats
Author(s) -
Dresow Bernd,
Albert Claudia,
Zimmermann Inge,
Nielsen Peter
Publication year - 1995
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840210432
Subject(s) - exhalation , lipid peroxidation , chemistry , medicine , endocrinology , vitamin e , siderosis , ubiquinol , lipidology , biochemistry , vitamin , antioxidant , clinical chemistry , mitochondrion , cytochrome c , coenzyme q – cytochrome c reductase , radiology
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 α‐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 α‐tocopherol decreased with progressive iron loading. In addition, a significant depletion in hepatic ubiquinol 9 and 10 was noted.