Photosensitized peroxidation of
membrane lipids has been implicated in skin pathologies such as
phototoxicity,
premature aging, and
carcinogenesis, and may play a role in the antitumor effects of
photodynamic therapy.
Lipid hydroperoxides (LOOHs) are prominent early products of photoperoxidation that typically arise via
singlet oxygen ((1)O(2)) attack. Nascent LOOHs can have several possible fates, including (i)
iron-catalyzed one-electron reduction to chain-initiating
free radicals, which exacerbate peroxidative damage, (ii) selenoperoxidase-catalyzed two-electron reduction to relatively innocuous
alcohols, and (iii) translocation to other membranes, where reactions noted in (i) or (ii) might take place. In addition, LOOHs, like other stress-associated
lipid metabolites/peroxidation products (e.g., arachidonate,
diacylglycerol,
ceramide, 4-hydroxynonenal), may act as signaling molecules. Intermembrane transfer of LOOHs may greatly expand their signaling range. When photogenerated rapidly and site-specifically, e.g., in mitochondria, LOOHs may act as early mediators of apoptotic cell death. This review will focus on these various aspects, with special attention to the role of LOOHs in photooxidative signaling.