Photo-pollution stress in skin: Traces of pollutants (PAH and particulate matter) impair redox homeostasis in keratinocytes exposed to UVA1

Sœur, Jérémie; Belaïdi, Jean-Philippe; Chollet, Christel; Denat, Laurence; Dimitrov, Ariane; Jones, Christophe; Perez, Philippe; Zanini, Martine; Zobiri, Olivia; Mezzache, Sakina; Erdmann, Dominique; Léreaux, Guillaume; Eilstein, Joan; Marrot, Laurent

doi:10.1016/j.jdermsci.2017.01.007

Cited by 107 publications

(141 citation statements)

References 49 publications

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“…For imaging, cells were plated in a 4-well glass chamber slide, treated with 1 mM NAC and/or 50 µg/mL PM 2.5 , and analyzed for intracellular and mitochondrial ROS production after staining with H 2 DCFDA and dihydrorhodamin 123 (DHR 123; Molecular Probes), respectively, for 30 min. Images of stained cells were generated by confocal microscopy as previously described (Kim and Yoo 2016; Soeur et al 2017). To detect ROS in zebrafish treated with NAC and/or PM 2.5 , they were incubated with 10 µM H 2 DCFDA for 30 min in the dark at 28.5 °C.…”

Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

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The skin is the largest organ of the human body and the one mostly exposed to outdoor contaminants. To evaluate the biological mechanisms underlying skin damage caused by fine particulate matter (PM2.5), we analyzed the effects of PM2.5 on cultured human keratinocytes and the skin of experimental animals. PM2.5 was applied to human HaCaT keratinocytes at 50 µg/mL for 24 h and to mouse skin at 100 µg/mL for 7 days. The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation. As a result, PM2.5 induced endoplasmic reticulum stress, mitochondrial swelling, and autophagy, and caused apoptosis in HaCaT cells and mouse skin tissue. The PM2.5-induced cell damage was attenuated by antioxidant N-acetyl cysteine, confirming that PM2.5 cellular toxicity was due to oxidative stress. These findings contribute to understanding of the pathophysiological mechanisms triggered in the skin by PM2.5, among which oxidative stress may play a major role.

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Section: Methodsmentioning

confidence: 99%

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

et al. 2018

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“…Environmental stressors are often considered a major contributor of skin hyperpigmentation, with UV as a prominent example . Recent evidence suggests that air pollutant containing melanogenic agents such as PAH could be another significant environmental stressor with hyperpigmentary effect .…”

Section: Discussionmentioning

confidence: 99%

“…Epidemiological evidence suggests that air pollution exposure is associated with ageing signs, pigment spots and incidence of eczema . However, establishing direct causal relationship between such long‐term accumulative exposure and phenotypical or biological consequences is often only possible using animal or in vitro models due to ethical considerations . A few recent studies have demonstrated that pollutant challenge induces oxidative stress and cellular damage in living skin equivalent (LSE) models .…”

Section: Introductionmentioning

confidence: 99%

“…However, establishing direct causal relationship between such long‐term accumulative exposure and phenotypical or biological consequences is often only possible using animal or in vitro models due to ethical considerations . A few recent studies have demonstrated that pollutant challenge induces oxidative stress and cellular damage in living skin equivalent (LSE) models . However, there is a lack of such in vitro model to simulate hyperpigmentation induced by non‐UV stressors.…”

Section: Introductionmentioning

confidence: 99%

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Niacinamide and 12‐hydroxystearic acid prevented benzo(a)pyrene and squalene peroxides induced hyperpigmentation in skin equivalent

Dong

Santhanam

et al. 2018

Experimental Dermatology

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Skin surface is constantly exposed to environmental and secreted stressors such as UV, air pollution and peroxidized sebum. The current study aims to use reconstructed human skin equivalents to demonstrate topical stressor‐induced hyperpigmentation and evaluate bioactives’ potential protective effect. Given that polycyclic aromatic hydrocarbons are representative airborne particle‐bound organic compounds with known relevance to pigmentation pathways, benzo(a)pyrene was selected as surrogate environmental toxin. On the other hand, squalene monohydroperoxides are well‐characterized sebum peroxidation product under UV and pollutant exposure, thus are used as another representative skin stressor. With 3‐day continuous exposure, 30 pmol/cm2 of benzo(a)pyrene and 3.4 nmol/cm2 of squalene monohydroperoxides induced significant viability loss, inflammatory response, and approximately 10 shades of pigmentation increase in pigmented living skin equivalents. At the same time, pretreatment and co‐treatment with 12‐hydroxystearic acid (12‐HSA, 20 μmol/L) or niacinamide (5 mmol/L) ameliorated such stressor‐induced consequences. Niacinamide was particularly effective against benzo(a)pyrene damage, probably as a substrate for important NAD+ dependent detoxification pathways, while 12‐HSA was potent against squalene monohydroperoxides through barrier enhancing, anti‐inflammatory, and anti‐oxidative mechanisms. In summary, topical stressor‐induced hyperpigmentation was achieved in vitro, with known bioactives showing protective benefits.

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“…This low‐grade, continuous (chronic) inflammation and upregulation of pro‐inflammatory mediators (IL‐6, IL‐8, TNF α …) are referred to as skin inflamm‐ageing . In addition to UV rays , the increase in air pollution over the years has been suspected to impact human skin . For example, cell membrane can be damaged from lipid oxidation induced by free radicals and cigarette smoke .…”

Section: Introductionmentioning

confidence: 99%

Vichy Thermal Spring Water (VTSW), a cosmetic ingredient of potential interest in the frame of skin ageing exposome: an in vitro study

Tacheau

Weisgerber

Fagot

et al. 2018

Intern J of Cosmetic Sci

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Photo-pollution stress in skin: Traces of pollutants (PAH and particulate matter) impair redox homeostasis in keratinocytes exposed to UVA1

Cited by 107 publications

References 49 publications

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis

Niacinamide and 12‐hydroxystearic acid prevented benzo(a)pyrene and squalene peroxides induced hyperpigmentation in skin equivalent

Vichy Thermal Spring Water (VTSW), a cosmetic ingredient of potential interest in the frame of skin ageing exposome: an in vitro study

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