Abstract
A number of agonists of the aryl hydrocarbon or dioxin receptor (AhR) are potent tumor promoters in rodent liver. The prototype compound is 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD). Tumor promotion by TCDD is likely to be AhR-mediated. Tumor promoters may affect the rate of division, terminal differentiation or death (apoptosis) of tumor precursor cells. The present paper reviews some of the effects of TCDD on liver cell homeostasis that have been observed under diverse experimental settings and discusses some of the possible underlying mechanisms.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
