Release of iron from ferritin in the presence of polyhydroxy metabolites of benzene i.e., hydroquinone (HQ) or 1,2,4-benzenetriol (BT) was studied in acetate buffer, pH 5.6. The release of iron from ferritin was quantitated by monitoring the formation of iron-ferrozine complex. The presence of hydroquinone (330 microM) did not result in the release of iron from ferritin, whereas the same concentration of BT resulted in the release of significant amounts of iron (3.2 microM/min) from ferritin. BT concentration-dependent increase in iron release from ferritin was observed although the increase was not linear with the concentration of BT. Under a N2 atmosphere the presence of BT resulted in the release of iron (2.1 microM/min) from ferritin. The presence of oxyradical scavengers i.e., albumin, catalase or superoxide dismutase significantly inhibited iron release from ferritin by BT. The iron released from ferritin by BT enhanced lipid peroxidation in rat brain homogenate and released aldehydic products from bleomycin-dependent degradation of DNA. Addition of BT to bone marrow lysate resulted in an increase of iron release as a function of time. These studies indicate that BT is a potent reductant of ferric iron of ferritin and also mobilizes and releases iron from ferritin core. The release of iron from bone marrow lysate by BT may be of toxicological significance as this could lead to disruption of intracellular iron homeostasis in bone marrow cells.
Acetates Albumins