Fine Particulate Matter-Induced Oxidative Stress Mediated by UVA-Visible Light Leads to Keratinocyte Damage

Abstract

The human skin is exposed to various environmental factors including solar radiation and ambient air pollutants. Although, due to its physical and biological properties, the skin efficiently protects the body against the harm of environmental factors, their excessive levels and possible synergistic action may lead to harmful effects. Among particulate matter present in ambient air pollutants, PM2.5 is of particular importance for it can penetrate both disrupted and intact skin, causing adverse effects to skin tissue. Although certain components of PM2.5 can exhibit photochemical activity, only a limited amount of data regarding the interaction of PM2.5 with light and its effect on skin tissue are available. This study focused on light-induced toxicity in cultured human keratinocytes, which was mediated by PM2.5 obtained in different seasons. Dynamic Light Scattering (DLS) and Atomic Force Microscopy (AFM) were employed to determine sizes of the particles. The ability of PM2.5 to photogenerate free radicals and singlet oxygen was studied using EPR spin-trapping and time-resolved singlet oxygen phosphorescence, respectively. Solar simulator with selected filters was used as light source for cell treatment to model environmental lightning conditions. Cytotoxicity of photoexcited PM2.5 was analyzed using MTT assay, PI staining and flow cytometry, and the apoptotic pathway was further examined using Caspase-3/7 assay and RT-PCR. Iodometric assay and JC-10 assay were used to investigate damage to cell lipids and mitochondria. Light-excited PM2.5 were found to generate free radicals and singlet oxygen in season-dependent manner. HaCaT cells containing PM2.5 and irradiated with UV-Vis exhibited oxidative stress features–increased peroxidation of intracellular lipids, decrease of mitochondrial membrane potential, enhanced expression of oxidative stress related genes and apoptotic cell death. The data indicate that sunlight can significantly increase PM2.5-mediated toxicity in skin cells.

Ultraviolet Light Protection: Is It Really Enough?

“…Although UV radiation is the most aggressive environmental agent, the role of pollution in damaging skin is significant. The impact of the combined exposure to pollutants and UV radiations on skin is due to their additive effects on oxinflammation [ 42 , 43 , 87 , 88 , 89 , 90 , 91 ]. PM, due to its composition, has been shown to interact with UV light [ 90 ].…”

“…The impact of the combined exposure to pollutants and UV radiations on skin is due to their additive effects on oxinflammation [ 42 , 43 , 87 , 88 , 89 , 90 , 91 ]. PM, due to its composition, has been shown to interact with UV light [ 90 ]. Poly aromatic hydrocarbons from PM and cigarette smoke can absorb UVA photons, and therefore be photoactivated by UV, exacerbating skin damage.…”

Dietary Intervention with Blackcurrant Pomace Protects Rats from Testicular Oxidative Stress Induced by Exposition to Biodiesel Exhaust

“…We believe that the observed differences in the oxidative toxicity between B7 DEE and SHB20 DEE resulted from the dissimilarity in the composition of the DEE-derived particles. Some studies investigating the exposure of animals to DEE particulate matter indicated that alteration of applied engine load changed the composition and biological reactivity of particles [ 59 , 60 ]. Indeed, the analysis of DEE from the combustion of both biofuels used in this study clearly demonstrated a difference in chemical characteristics of emissions from the two tested fuels [ 26 , 61 , 62 ].…”

Effects of Air Pollution on Cellular Senescence and Skin Aging

“…PAH is an activator of AhR in melanocytes and keratinocytes and exposition of the skin to this chemical can influence epidermal turnover, melanogenesis, and differentiation [ 9 , 86 ]. PAH have synergistic effect with UVA and both contribute to skin carcinogenesis and to the appearance of skin pigmentation disorders such as senile lentigines [ 5 , 53 , 70 , 92 , 109 , 110 ]. Interestingly, exposure of melanocytes to PM induces apoptosis through cytochrome C release and activation of caspase-3 [ 111 ].…”