Chemistry Institute at São Carlos, University of São Paulo, Av. Trabalhador São Carlesense 400 CP 780, CEP 13560-970, São Carlos, SP, Brazil.
Food Funct. 2012 May;3(5):487-502. doi: 10.1039/c2fo10246c. Epub 2012 Mar 12.
Riboflavin, vitamin B₂, and flavins (as riboflavin building blocks or degradation products) are efficient photosensitizers inducing oxidative damage to light-exposed tissue and food by substrate-dependent mechanisms, for which protection is offered by specific nutrients. Phenolic and N-heterocyclic amino acids and their peptides and proteins deactivate triplet-excited state riboflavin in diffusion controlled processes, efficiently competing with deactivation by oxygen, resulting in direct (so called Type I) protein degradation through electron transfer or proton-coupled electron transfer. In light-exposed tissue, such often long lived protein radicals may as primary photoproducts initiate lipid and vitamin oxidation. In contrast, for lipid systems, oxygen deactivation of triplet-excited state riboflavin, resulting in formation of singlet oxygen, is under aerobic conditions faster than direct deactivation by lipids, which otherwise under anaerobic conditions occurs as hydrogen atom transfer from polyunsaturated lipids to triplet riboflavin. Singlet oxygen adds to unsaturated lipids and forms lipid hydroperoxides as primary lipid oxidation products or oxidizes proteins (Type II mechanism). Carotenoids seem not to deactivate triplet riboflavin, while chromanols like vitamin E and plant polyphenols are efficient in such deactivation yielding protection of proteins and lipids by these phenols. Indirect protection against the triplet reactivity of riboflavin is further important for polyphenols as riboflavin singlet excited state quenchers in effectively preventing riboflavin intersystem crossing to yield the reactive triplet state. Riboflavin photosensitization becomes critical for degradation of proteins, unsaturated lipids, and folate, thiamine, ascorbate and other vitamins during light exposure of food during storage. For skin, eye and other tissue exposed to high intensity light, dietary polyphenols like flavonoids are important in direct protection against photosensitized oxidation, while dietary carotenoids may yield protection through inner-filter effects, through scavenging of radicals resulting from Type I photosensitization, and through quenching of singlet oxygen formed in Type II photosensitization. Both carotenoids and polyphenols accordingly counteract the degenerative effect induced by riboflavin exposed to light, although by different mechanisms.
核黄素，维生素 B₂，和黄素（作为核黄素的结构单元或降解产物）是有效的光敏剂，通过底物依赖的机制诱导暴露于光的组织和食物发生氧化损伤，而特定的营养物质为其提供了保护。酚类和杂环氨基酸及其肽和蛋白质通过扩散控制过程使三重激发态核黄素失活，有效地与氧的失活竞争，导致通过电子转移或质子偶联电子转移直接（所谓的 I 型）蛋白质降解。在暴露于光的组织中，这种通常寿命较长的蛋白质自由基可能作为初级光产物引发脂质和维生素氧化。相比之下，对于脂质系统，在有氧条件下，三重激发态核黄素的氧失活导致单线态氧的形成，比脂质的直接失活要快，而在无氧条件下，单线态氧通过从多不饱和脂质向三重态核黄素转移氢原子发生。单线态氧与不饱和脂质加成并形成脂质氢过氧化物作为初级脂质氧化产物，或氧化蛋白质（II 型机制）。类胡萝卜素似乎不能使三重态核黄素失活，而色满醇如维生素 E 和植物多酚在这种失活中非常有效，从而通过这些酚类物质保护蛋白质和脂质。间接保护核黄素的三重态反应性对于多酚类物质也很重要，因为它们是核黄素单线激发态猝灭剂，可有效防止核黄素的系间窜越以产生反应性三重态。在食物储存过程中暴露于光时，核黄素的光敏化对于蛋白质、不饱和脂质和叶酸、硫胺素、抗坏血酸和其他维生素的降解变得至关重要。对于暴露于高强度光的皮肤、眼睛和其他组织，饮食中的多酚类物质如类黄酮在直接保护免受光敏氧化方面很重要，而饮食中的类胡萝卜素可以通过内滤效应、通过清除 I 型光敏化产生的自由基以及通过猝灭 II 型光敏化中形成的单线态氧来提供保护。类胡萝卜素和多酚类物质都相应地抵消了由暴露于光的核黄素引起的退行性效应，尽管它们的机制不同。
