Journal
JOURNAL OF COMPARATIVE PHYSIOLOGY B-BIOCHEMICAL SYSTEMS AND ENVIRONMENTAL PHYSIOLOGY
Volume 175, Issue 4, Pages 221-230Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00360-005-0483-3
Keywords
dioxin; TCDD; aryl hydrocarbon receptor (AhR); CYP1A1
Categories
Ask authors/readers for more resources
A highly persistent trace environmental contaminant and one of the most potent toxicants known is dioxin (2,3,7,8-tetrachlorodibenzo-para-dioxin or TCDD). TCDD induces a broad spectrum of biological responses, including induction of cytochrome P-450 1A1 (CYP1A1), disruption of normal hormone signaling pathways, reproductive and developmental defects, immunotoxicity, liver damage, wasting syndrome, and cancer. Its classification was upgraded from possible human carcinogen (group 2B) to human carcinogen (group 1) by the International Agency for Research on Cancer (IARC) in 1997. Exposure to TCDD may also cause changes in sex ratio, and tumor promotion in other animals. Because of the growing public and scientific concern, toxicological studies have been initiated to analyze the short- and long-term effects of dioxin. TCDD brings about a wide variety of toxic and biochemical effects via aryl hydrocarbon receptor (AhR)mediated signaling pathways. Essential steps in this adaptive mechanism include AhR binding or ligand in the cytoplasm of cells associated with two molecules of chaperone heatshock protein (Hsp90) and AhR interactive protein, translocation of the receptor to the nucleus, dimerization with the Ah receptor nuclear translocator, and binding of this heterodimeric transcription factor (present in CYP1A) to dioxin-responsive elements upstream of promoters that regulate the expression of genes involved in xenobiotic metabolism.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available