Abstract
The pathways of photoreactivity of some nonsteroidal antiinflammatory drugs (NSAID), i.e. propionic acid derivatives indicated in a clinical picture as phototoxic and/or photoallergic, are discussed in a general oversimplified scheme. The NSAID photosensitizing activity, estimated from the ability to induce red blood cell lysis, was found to be dependent on the quantum yield of decarboxylation, which in turn determines the superoxide anion formation, on free radical reactivity and on singlet oxygen production efficiency. An investigation into the NSAID photoinduced cell damage in erythrocytes from various mammalian species, erythrocyte ghosts and unilamellar liposomes, evidenced the role played by membrane proteins and phospholipids. To inhibit phototoxic effects, some systems, including β-cyclodextrin and cupric Ion and its complexes with bio-functionalized ligands, were considered for their ability in protecting cell membranes from the damage, which is photoinduced by superoxide anion, free radicals and singlet oxygen.
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