Fe allocation in liver during early stages of endotoxemia in Fe-overload rats.

The hypothesis of this study was that alterations in Fe distribution triggered by lipopolysaccharide (LPS) administration were affected in vivo by Fe overload. Lipopolysaccharide treatment by itself significantly decreased Fe content in serum and increased the blood NO-hemoglobin (NO-Hb) EPR signal and nitrotyrosine protein content in liver, as compared to values in control animals. Fe overload (produced by Fe-dextran ip administration) caused an increase, as compared to values in control animals, in Fe content in serum, and a significant enhancement in ferritin (Ft) content, Fe content in Ft, the labile Fe pool (LIP), and the protein carbonyl content in the liver.

Ferritin-dependent radical generation in rat liver homogenates.

The hypothesis of this study was that mammalian ferritin (FER) has the ability of releasing Fe in the tissue to catalyze the generation of free radicals, such as ascorbyl (A) and hydroxyl radical (OH), that might lead to the damage of FER itself. The rat liver homogenates exhibited an electron paramagnetic resonance (EPR) signal with the spectral features (a(H)=1.88 G, g=2.