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Mechanism of action[edit]
TCDD and dioxin-like compounds act via a specific receptor present in all cells: the aryl hydrocarbon (AH) receptor.[18][19][20] This receptor is a transcription factor which is involved in expression of genes; in fact it has been shown that high doses of TCDD either increase or decrease the expression of several hundred genes in rats.[21] Genes of enzymes activating the breakdown of foreign and often toxic compounds are classic examples of such genes. TCDD increases the enzymes breaking down, e.g., carcinogenic polycyclic hydrocarbons such as benzo(a)pyrene.[22]
These polycyclic hydrocarbons also activate the AH receptor, but less than TCDD and only temporarily.[22] Even many natural compounds present in vegetables cause some activation of the AH receptor.[23] This phenomenon can be viewed as adaptive and beneficial, because it protects the organism from toxic and carcinogenic substances. Excessive and persistent stimulation of AH receptor, however, leads to a multitude of adverse effects.[22]
The physiological function of the AH receptor has been the subject of continuous research. One obvious function is to increase the activity of enzymes breaking down foreign chemicals or normal chemicals of the body as needed. There may be other functions, however, related to growth of various organs or other regulatory functions. The AH receptor is phylogenetically highly conserved transcription factor with a history of at least 500 million years, and found in all vertebrates, and its ancient analogs are important regulatory proteins even in more primitive species.[20] In fact, knock-out animals with no AH receptor are prone to illness and developmental problems.[20] Taken together, this implies the necessity of a basal degree of AH receptor activation to achieve normal physiological function.
While the mutagenic and genotoxic effects of TCDD are sometimes disputed[11] and sometimes confirmed[24] it does foster the development of cancer. Its main action in causing cancer is cancer promotion; it promotes the carcinogenicity initiated by other compounds. Very high doses may, in addition, cause cancer indirectly; one of the proposed mechanisms is oxidative stress and the subsequent oxygen damage to DNA.[12] There are other explanations such as endocrine disruption or altered signal transduction.[11][25] The endocrine disrupting activities seem to be dependent on life stage, being anti-estrogenic when estrogen is present (or in high concentration) in the body, and estrogenic in the absence of estrogen.[26]

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