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Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands

by 1,2,3,* and 1,2
1
Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan
2
Research and Clinical Center for Yusho and Dioxin, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan
3
Division of Skin Surface Sensing, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashiku, Fukuoka 812-8582, Japan
*
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2019, 16(23), 4864; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph16234864
Received: 21 October 2019 / Revised: 26 November 2019 / Accepted: 2 December 2019 / Published: 3 December 2019
(This article belongs to the Special Issue Environment, Endocrine Disruptors and Cutaneous Effects)
Dioxins and dioxin-like compounds are environmental pollutants that are hazardous to human skin. They can be present in contaminated soil, water, and air particles (such as ambient PM2.5). Exposure to a high concentration of dioxins induces chloracne and hyperpigmentation. These chemicals exert their toxic effects by activating the aryl hydrocarbon receptor (AHR) which is abundantly expressed in skin cells, such as keratinocytes, sebocytes, and melanocytes. Ligation of AHR by dioxins induces exaggerated acceleration of epidermal terminal differentiation (keratinization) and converts sebocytes toward keratinocyte differentiation, which results in chloracne formation. AHR activation potently upregulates melanogenesis in melanocytes by upregulating the expression of melanogenic enzymes, which results in hyperpigmentation. Because AHR-mediated oxidative stress contributes to these hazardous effects, antioxidative agents may be potentially therapeutic for chloracne and hyperpigmentation. View Full-Text
Keywords: chloracne; hyperpigmentation; dioxin; aryl hydrocarbon receptor; reactive oxygen species; epidermal terminal differentiation; melanocytes chloracne; hyperpigmentation; dioxin; aryl hydrocarbon receptor; reactive oxygen species; epidermal terminal differentiation; melanocytes
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MDPI and ACS Style

Furue, M.; Tsuji, G. Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands. Int. J. Environ. Res. Public Health 2019, 16, 4864. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph16234864

AMA Style

Furue M, Tsuji G. Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands. International Journal of Environmental Research and Public Health. 2019; 16(23):4864. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph16234864

Chicago/Turabian Style

Furue, Masutaka, and Gaku Tsuji. 2019. "Chloracne and Hyperpigmentation Caused by Exposure to Hazardous Aryl Hydrocarbon Receptor Ligands" International Journal of Environmental Research and Public Health 16, no. 23: 4864. https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph16234864

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