Ethane exhalation and vitamin E/ubiquinol status as markers of lipid peroxidation in ferrocene iron—loaded rats

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.