The epigenetic effects of dioxins

• Published in: Dioxin pp. 113 - 128
• Main Authors: Heyliger, Simone O., Saulsbury, Marilyn D.
• Format: Book Chapter
• Language: English
• Published: CRC Press 2020
• Edition: 1
• Subjects: DNA Modification; PCB Congener; AHR Function; Endocrine Disruption; CXCR4 Gene; ARNT; AHR; Histone Modifications; BRCA1; Ng TEQ; BRCA3; OCDD; Aryl Hydrocarbon Receptor; DNA Methylation; DNA Methylation Status; DNA Methyl Transferase; ERBB2; Global DNA Hypermethylation; PCR Amplify 16S rRNA Gene; CREB Level; ULK1; Neuroblastoma Ras Oncogene; Steroid Receptor Coactivator; SRC-1
• ISBN: 9781138047242; 1138047244
• DOI: 10.1201/9781315170961-7

Environmental epigenetics is a relatively new area of discipline and represents a new approach for conducting risk assessments. To date, most focus studies have centered around the epigenetics of heavy metals such as arsenic, mercury, lead, and calcium. The induction of different epigenetic mechanisms in various tissues or different cell types may offer insight into complex nature of dioxin toxicity and aryl hydrocarbon receptor functions. Mounting evidence indicate that dioxins and dioxin-like compounds can induce neurological changes in the developing fetus and infant. The revelation that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can alter global methylation status engenders potential questions related to how dioxin promotes tumorigenesis. Dioxins are structurally diverse polyhalogenated aromatic hydrocarbons that include polychlorinated dibenzodioxins, polychlorinated dibenzofurans, and polychlorinated biphenyls. Toxicologists have long recognized that TCDD and dioxin-like polychlorinated biphenyls haves a suppressive effect on the immune system.