Translocation as a means of disseminating lipid hydroperoxide-induced oxidative damage and effector action.

Lipid hydroperoxides (LOOHs) generated in cells and lipoproteins under oxidative pressure may induce waves of damaging chain lipid peroxidation near their sites of origin if O2 is readily available and antioxidant capacity is overwhelmed. However, recent studies have demonstrated that chain induction is not necessarily limited to a nascent LOOH's immediate surroundings but can extend to other cell membranes or lipoproteins by means of LOOH translocation through the aqueous phase. Mobilization and translocation can also extend the range of LOOHs as redox signaling molecules and in this sense they could act like the small, readily diffusible inorganic analogue H2O2, which has been studied much more extensively in this regard. In this article, basic mechanisms of free-radical- and singlet-oxygen-mediated LOOH formation and one-electron and two-electron LOOH reduction pathways and their biological consequences are reviewed. The first studies to document spontaneous and protein-assisted LOOH transfer in model systems and cells are described. Finally, LOOH translocation is discussed in the context of cytotoxicity vs detoxification and expanded effector action, i.e., redox signaling activity.