Reif D W, Beales I L, Thomas C E, Aust S D
Department of Biochemistry, Michigan State University, East Lansing 48824.
Toxicol Appl Pharmacol. 1988 May;93(3):506-10. doi: 10.1016/0041-008x(88)90054-3.
Diquat toxicity is proposed to be mediated through the generation of active oxygen species; however, the exact role of active oxygen in toxicity is not known. The generation of damaging oxygen radicals requires transition metals such as iron. In vitro studies have shown that redox cycling of diquat results in the release of iron from ferritin, thus, increasing the potential for active oxygen species generation. We sought to determine if diquat administration to male Sprague-Dawley rats would result in the release of iron from ferritin in vivo. Rats were treated with diquat dibromide (20 mg/kg body weight) and the effect on the iron distribution in liver was determined. The results show that diquat-treated animals had increased levels of hepatic low molecular weight chelatable iron (LMWC-Fe) and decreased levels of hepatic ferritin iron when compared to saline-treated animals. These results suggest that diquat toxicity may be associated with the release of iron from ferritin in vivo and that iron release from ferritin may be a process common to other free radical mediated toxicities.
