Chloracne and hyperpigmentation caused by exposure to hazardous aryl hydrocarbon receptor ligands

Research output: Contribution to journalReview article

Abstract

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 ofAHR 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.

Original languageEnglish
Article number4864
JournalInternational journal of environmental research and public health
Volume16
Issue number23
DOIs
Publication statusPublished - Dec 1 2019

Fingerprint

Chloracne
Aryl Hydrocarbon Receptors
Hyperpigmentation
Dioxins
Melanocytes
Ligands
Keratinocytes
Environmental Pollutants
Skin
Poisons
Ligation
Oxidative Stress
Up-Regulation
Soil
Air
Water
Enzymes
Therapeutics

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Cite this

@article{fbe6aa235311440f889bdf02f27dfcd0,
title = "Chloracne and hyperpigmentation caused by exposure to hazardous aryl hydrocarbon receptor ligands",
abstract = "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 ofAHR 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.",
author = "Masutaka Furue and Gaku Tsuji",
year = "2019",
month = "12",
day = "1",
doi = "10.3390/ijerph16234864",
language = "English",
volume = "16",
journal = "International Journal of Environmental Research and Public Health",
issn = "1661-7827",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "23",

}

TY - JOUR

T1 - Chloracne and hyperpigmentation caused by exposure to hazardous aryl hydrocarbon receptor ligands

AU - Furue, Masutaka

AU - Tsuji, Gaku

PY - 2019/12/1

Y1 - 2019/12/1

N2 - 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 ofAHR 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.

AB - 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 ofAHR 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.

UR - http://www.scopus.com/inward/record.url?scp=85076231063&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85076231063&partnerID=8YFLogxK

U2 - 10.3390/ijerph16234864

DO - 10.3390/ijerph16234864

M3 - Review article

C2 - 31816860

AN - SCOPUS:85076231063

VL - 16

JO - International Journal of Environmental Research and Public Health

JF - International Journal of Environmental Research and Public Health

SN - 1661-7827

IS - 23

M1 - 4864

ER -