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 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.
Highlights
Health problems induced by environmental pollutants are an important issue
Because aryl hydrocarbon receptor (AHR)-mediated oxidative stress contributes to these hazardous effects, antioxidative agents may be potentially therapeutic for chloracne and hyperpigmentation
In Japan, chloracne and hyperpigmentation are present in Yusho, which occurred in Japan in 1968 by mass food poisoning with high concentrations of polychlorinated dibenzofurans (PCDFs) and related compounds [12,14,15]
Summary
Environmental polycyclic and halogenated aromatic hydrocarbons, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and benzo[a]pyrene (BaP) are high-affinity ligands for aryl hydrocarbon receptors (AHRs), namely, dioxin receptor [1,2,3,4,5] To sense these chemicals, AHR is abundantly expressed in skin cells, including epidermal keratinocytes [1,2,3,4,5]. In Japan, chloracne and hyperpigmentation are present in Yusho, which occurred in Japan in 1968 by mass food poisoning with high concentrations of PCDFs and related compounds [12,14,15]. We will review the current evidence on chloracne and hyperpigmentation induced by AHR activation
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