mainly due to the activation of nicotinamide adenine dinucleotide
phosphate (NADPH) oxidase, xanthine oxidase, and the mitochondrial electron transport system,45 and it is responsible for protein and DNA oxidation.8 Increase in skin temperatures is also associated with chronic inflammation and a pro-angiogenic environment characterized by an increased VEGF to thrombospondin
(TSP)-1 and 2 ratio.46 Finally, heat-activation of transient receptor potential vanilloid-1 (TRPV-1) mediates the expression of MMP-1,47,48 opening a potential role for TRPV-1 inhibitors to be used to prevent heat-induced skin aging.
Visible Light
The visible part of the solar spectrum is used for general illumination
and is defined by the electromagnetic radiation that is visible to the human eye (400 nm - 760 nm).49 Visible light accounts for the remaining 38.9% of the solar radiation reaching the earth’s surface,6 and is able to penetrate the dermis
and generate heat after being absorbed. While there is now substantial evidence to indicate that UV, IR, and heat all influence solar-aging, the contribution of visible light to skin damage is less well understood,1,7 due in part to the lack of light sources that emit in the visible spectrum (without UV or IR contamination).50
Recent experiments have shown that visible light can increase the production of ROS, stimulate the production of pro-inflammatory
cytokines, and upregulate the expression of MMP-1 in humans.51 In addition, a potential role of visible light in DNA damage has been suggested by Kielbassa et al,52 who estimated
that 10% of the total DNA oxidation is associated with
