Resumen–En este artículo se discute el descubrimiento del litopón fosforescente en dibujos a la acuarela por el artista americano John La Farge, fechados de 1890 a 1905, y la historia del litopón en la industria de los pigmentos a finales del Siglo XIX y principios del Siglo XX. A pesar de tener muchas cualidades deseables para su uso en pintura para acuarela o pinturas al óleo blancas, el desarrollo del litopón como pigmento para artistas fue obstaculizado por su tendencia a oscurecerse con la luz solar. Su disponibilidad para los artistas y su adopción por ellos sigue siendo poco clara, ya que por lo general los catálogos comerciales de los coloristas no eran explícitos al describir si los pigmentos blancos contenían litopón. Además, el litopón se puede confundir con blanco de plomo durante el examen visual, y su fosforescencia de corta duración puede ser fácilmente pasada por alto por el observador desinformado. A la fecha, el litopón fosforescente ha sido documentado solamente en otra obra mas: una acuarela por Van Gogh. Además de la historia de la fabricación del litopón, el artículo detalla el mecanismo para su fosforescencia, y su identificación con la ayuda de espectroscopía de Raman, y de espectrofluorimetría.
As mentioned above, these oxide NPs are harmful in part because both anatase and rutile forms are semiconductors and produce ROS. Particularly, P25 kind has band-gap energies estimated of 3.2 and 3.0 eV, equivalent to radiation wavelengths of approximately 388 and 414 nm, respectively. Irradiation at these wavelengths or below produces a separation of charge, resulting in a hole in the valence band and a free electron in the conduction band, due to the electron movement from the valence to conduction bands. These hole–electron pairs generate ROS when they interact with H2O or O2 [43,44]. It was described that they can cause an increase in ROS levels after exposure to UV-visible light [45]. The NBT assay in the studied samples showed that bare P25TiO2NPs produce a large amount of ROS, which is drastically reduced by functionalization with vitamin B2 (Fig. 5). This vitamin, also known as riboflavin, was discovered in 1872 as a yellow fluorescent pigment, [46] but its function as an essential vitamin for humans was established more than sixty years later, and its antioxidant capacity was not studied until the end of the XX century [47,48]. This antioxidant role in cells is partially explained because the glutathione reductase enzyme (GR) requires it for good functionality. This enzyme is the one in charge of the conversion of oxidized glutathione to its reduced form which acts as a powerful inner antioxidant and can quench the ROS [49,50]. The cost of this action is that the glutathione is converted to the oxidized form and needs to be recovered by the GR. Consequently, the cells need more vitamin B2. Another glutathione action is the protection against hydroperoxide. This activity is also mediated by riboflavin. Therefore, local delivery of this vitamin seems to significantly help the cells in their fight to keep the oxidative balance, once they are exposed to high levels of ROS.
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