TCDD Toxicity Mediated by Epigenetic Mechanisms
Authors: Patrizi B., Siciliani de Cumis M.
Autors Affiliation: Natl Inst Opt, Natl Res Council INO CNR, I-50019 Sesto Fiorentino, Italy. European Lab Nonlinear Spect LENS, Via Nello Carrara 1, I-50019 Sesto Fiorentino, Italy Italian Space Agcy Contrada Terlecchia Snc, I-75100 Matera, Italy
Abstract: Dioxins are highly toxic and persistent halogenated organic pollutants belonging to two families i.e., Polychlorinated Dibenzo-p-Dioxins (PCDDs) and Polychlorinated Dibenzo Furans (PCDFs). They can cause cancer, reproductive and developmental issues, damage to the immune system, and can deeply interfere with the endocrine system. Dioxins toxicity is mediated by the Aryl-hydrocarbon Receptor (AhR) which mediates the cellular metabolic adaptation to these planar aromatic xenobiotics through the classical transcriptional regulation pathway, including AhR binding of ligand in the cytosol, translocation of the receptor to the nucleus, dimerization with the AhR nuclear translocator, and the binding of this heterodimeric transcription factor to dioxin-responsive elements which regulate the expression of genes involved in xenobiotic metabolism. 2,3,7,8-TCDD is the most toxic among dioxins showing the highest affinity toward the AhR receptor. Beside this classical and well-studied pathway, a number of papers are dealing with the role of epigenetic mechanisms in the response to environmental xenobiotics. In this review, we report on the potential role of epigenetic mechanisms in dioxins-induced cellular response by inspecting recent literature and focusing our attention on epigenetic mechanisms induced by the most toxic 2,3,7,8-TCDD.
Journal/Review: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume: 19 (12) Pages from: 4101-1 to: 4101-15
KeyWords: 2,3,7,8-TCDD; Dioxins; Environmental xenobiotics; Epigenetic mechanismsDOI: 10.3390/ijms19124101Citations: 16data from “WEB OF SCIENCE” (of Thomson Reuters) are update at: 2021-03-07References taken from IsiWeb of Knowledge: (subscribers only)Connecting to view paper tab on IsiWeb: Click hereConnecting to view citations from IsiWeb: Click here