Abstract
Chloracne is the major skin symptom caused by dioxin intoxication. Dioxin activates the aryl hydrocarbon receptor (AHR)–cytochrome p450 1A1 (CYP1A1) system, generates oxidative stress, and induces hyperkeratinization of keratinocytes and sebocytes leading to chloracne. Nuclear factor-erythroid 2-related factor-2 (NRF2) is a master switch that induces the expression of various antioxidative enzymes, such as heme oxygenase-1. Cinnamaldehyde is an antioxidant phytochemical that inhibits AHR–CYP1A1 signaling and activates the NRF2–antioxidative axis. The cinnamaldehyde-containing Kampo herbal medicine Keishibukuryogan is capable of improving chloracne in Yusho patients who are highly contaminated with dioxin. Agents with dual functions in promoting AHR–CYP1A1 inhibition and NRF2 activation may be useful for managing dioxin-related health hazards.
Highlights
Health problems associated with environmental pollutants are an important issue
We focus on the aryl hydrocarbon receptor (AHR) signaling related to chloracne and highlight its potential treatment with an nuclear factor-erythroid 2-related factor-2 (NRF2) agonist
Chloracne is a devastating skin symptom induced by exposure to high concentrations of dioxins and other hazardous compounds
Summary
Environmental polycyclic aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, polychlorinated dibenzofuran, and benzo(a)pyrene (BaP) are high-affinity ligands for the aryl hydrocarbon receptor (AHR) or dioxin receptor [1,2,3,4]. These chemical compounds strongly activate AHR, generate reactive oxygen species (ROS), and induce the production of inflammatory cytokines in various tissues including skin [1,2,3,4]. We focus on the AHR signaling related to chloracne and highlight its potential treatment with an NRF2 agonist
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