Skin Damage Mechanisms Related to Airborne Particulate Matter Exposure.
Epidemiological studies suggest a correlation between increased airborne particulate matter (PM) and adverse health effects. The mechanisms of PM-health effects are believed to involve oxidative stress and inflammation. To evaluate the ability of PM promoting skin tissue damage, one of the main organs exposed to outdoor pollutants, we analyzed the effect of concentrated ambient particles (CAPs) in a reconstructed human epidermis (RHE) model. RHE tissues were exposed to 25 or 100 µg/ml CAPs for 24 or 48 h. Data showed that RHE seems to be more susceptible to CAPs-induced toxicity after 48 h exposure than after 24 h. We found a local reactive O(2) species (ROS) production increase generated from metals present on the particle, which contributes to lipids oxidation. Furthermore, as a consequence of altered redox status, NFkB nucleus translocation was increase upon CAPs exposure, as well as cyclooxygenase 2 and cytochrome P450 levels, which may be involved in the inflammatory response initiated by PM. CAPs also triggered an apoptotic process in skin. Surprisingly, by transition electron microscopy analysis we showed that CAPs were able to penetrate skin tissues. These findings contribute to the understanding of the cutaneous pathophysiological mechanisms initiated by CAPs exposure, where oxidative stress and inflammation may play predominant roles.
*Institute of Biochemistry and Molecular Medicine (IBIMOL-UBA-CONICET), Pharmacy and Biochemistry School, University of Buenos Aires, Buenos Aires, Argentina;
Natalia D
ND
Magnani
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy;
Ximena M
XM
Muresan
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy;
Giuseppe
G
Belmonte
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy;
Franco
F
Cervellati
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy;
Claudia
C
Sticozzi
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy;
Alessandra
A
Pecorelli
Department of Neuroscience, Medical and Surgical Sciences. University of Siena, Siena, Italy; and.
Clelia
C
Miracco
*Institute of Biochemistry and Molecular Medicine (IBIMOL-UBA-CONICET), Pharmacy and Biochemistry School, University of Buenos Aires, Buenos Aires, Argentina;
Timoteo
T
Marchini
*Institute of Biochemistry and Molecular Medicine (IBIMOL-UBA-CONICET), Pharmacy and Biochemistry School, University of Buenos Aires, Buenos Aires, Argentina;
Pablo
P
Evelson
Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy; Department of Food and Nutrition, Kyung Hee University, Seoul, South Korea vlcgpp@unife.it.
Giuseppe
G
Valacchi
D002478:Cells, Cultured; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics; D006801:Humans; D007249:Inflammation / Q000150:complications; D053582:Interleukin-1alpha / Q000502:physiology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D018384:Oxidative Stress; D052638:Particulate Matter / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000648:ultrastructure
D053582:Interleukin-1alpha; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; C495635:NFE2L2 protein, human; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D007770:L-Lactate Dehydrogenase; C569463:CYP1A1 protein, human; D019363:Cytochrome P-450 CYP1A1
air pollution; cutaneous tissues; inflammation; oxidative damage; particulate matter