The environmental pollutant 2,3,7,8‐tetrachlorodibenzo‐ρ‐dioxin (TCDD)
is the prototype of a large number of nongenotoxic environmental
carcinogens, dietary phytochemicals and endogenous metabolites that act
via binding the aryl hydrocarbon receptor (AHR). However, the
mechanism(s) of carcinogenesis by these compounds is still unclear. We
confirmed that TCDD‐liganded AHR massively upregulates CYP1A1, CYP1A2
and CYP1B1 in many mammalian organs.
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