Abstract
Photochemoprevention can be a valuable approach to counteract the damaging effects of environmental stressors (e.g., UV radiations) on the skin. Pigments are bioactive molecules, greatly attractive for biotechnological purposes, and with promising applications for human health. In this context, marine microalgae are a valuable alternative and eco-sustainable source of pigments that still need to be taken advantage of. In this study, a comparative in vitro photochemopreventive effects of twenty marine pigments on carcinogenic melanoma model cell B16F0 from UV-induced injury was setup. Pigment modulation of the intracellular reactive oxygen species (ROS) concentration and extracellular release of nitric oxide (NO) was investigated. At the cell signaling level, interleukin 1-β (IL-1β) and matrix metallopeptidase 9 protein (MMP-9) protein expression was examined. These processes are known to be involved in the signaling pathway, from UV stress to cancer induction. Diatoxanthin resulted the best performing pigment in lowering MMP-9 levels and was able to strongly lower IL-1β. This study highlights the pronounced bioactivity of the exclusively aquatic carotenoid diatoxanthin, among the others. It is suggested increasing research efforts on this molecule, emphasizing that a deeper integration of plant ecophysiological studies into a biotechnological context could improve the exploration and exploitation of bioactive natural products.
Highlights
Skin represents a barrier between organism and environment, being exposed to direct oxidative injury determined by ultraviolet (UV) radiation, representing the first level of immune defense
UV-radiation induces in skin tissue an increased generation of intracellular reactive oxygen species (ROS), an over-expression of matrix metalloproteinases (MMPs), and the production of proinflammatory cytokines (Interleukins-IL) through extracellular nitric oxide (NO) signaling [3]
An increase of intracellular ROS induces the phosphorylation of protein kinases through mitogen-activated protein kinases (MAPK) signaling pathway which directly promotes the phosphorylation of the activator protein-1 (AP-1) complex, up-regulating the expression of MMPs [4]
Summary
Skin represents a barrier between organism and environment, being exposed to direct oxidative injury determined by ultraviolet (UV) radiation, representing the first level of immune defense. An acute UV exposure causes short- and long-term deleterious effects on human epidermis, such as sunburn, connective tissue deterioration, DNA injury, and immune suppression [1]. Chronic exposure to UV radiation can be deleterious, leading to various long-term damaging effects, including skin aging (photoaging) or skin cancer (photocarcinogenesis). UV-radiation induces in skin tissue an increased generation of intracellular reactive oxygen species (ROS), an over-expression of matrix metalloproteinases (MMPs), and the production of proinflammatory cytokines (Interleukins-IL) through extracellular nitric oxide (NO) signaling [3]. An increase of intracellular ROS induces the phosphorylation of protein kinases through mitogen-activated protein kinases (MAPK) signaling pathway which directly promotes the phosphorylation of the activator protein-1 (AP-1) complex, up-regulating the expression of MMPs [4]
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