RESUMO
We report here on a retinoid model of the phenomenon discovered in 1980, in which ceroid-lipofuscin cytosomes (CLC) increased their intrinsic fluorescence when exposed to fluorescence-exciting (lambda(ex)=365nm) ultraviolet (UV) light. We modeled this effect in vitro, irradiating a methanolic solution of retinyl palmitate (RP) either synthetic or extracted from the aged rat liver retinoid. Following our model, the mechanism of this phenomenon can be explained by the photodecomposition of RP during fluorescence. Palmitic acid (PA) that quenched fluorescence was separated by photohydrolysis and some products of RP photodegradation shifted absorption spectra towards the fluorescence-exciting UV band compared with the absorption spectrum of the initial RP. The total intensity of intrinsic fluorescence at 490nm of RP photodegradation products increased several times, because relative absorption at 365 nm wavelength was higher. We report here also the established chemical formulae of two retinoids, derivatives of RP photohydrolysis tentatively called R(368) and R(346). R(368) was determined as anhydroretinol, a naturally occurring intracellular messenger in the transduction pathway of retinoids regulating growth inhibition in lymphoid line cells. Retinoid R(346) was determined to be a methanolic intermediate of RP photodegradation (4,5-dihydro-5-methoxy-Anhydroretinol).
