Endo
crine-active che
micals alter or
mi
mic physiological hor
mones. These co
mpounds are reported to originate fro
m a wide variety of sources, and recent studies have shown widespread hu
man exposure to several of these co
mpounds. Given the role of the sex steroid hor
mone, estradiol, in hu
man breast cancer causation, endo
crine-active che
micals which interfere with estrogen signaling constitute one potential factor contributing to the high incidence of breast cancer. Thus, the ai
m of this review is to exa
mine several co
mmon endo
crine-active che
micals and their respective roles in breast cancer causation or prevention. The plastic co
mponent, bisphenol A (BPA), the synthetic estrogen, diethylstilbestrol (DES), the by-product of organic co
mbustion, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the soy co
mponent, genistein, and the red grape phytoalexin, resveratrol, have so
me degree of structural si
milarities to each other and estradiol. However, despite these structural si
milarities, the
m>in vitrom> and
m>in vivom> properties of each of these che
micals vary greatly in ter
ms of breast cancer causation and prevention. Early life exposure to BPA and DES increases rodent susceptibility to che
mically induced
ma
mmary carcinogenesis, presu
mably through retardation of nor
mal
ma
mmary gland
maturation and/or disrupting the ratio of cell proliferation and apoptosis in the
ma
mmary gland. On the other hand, early exposures to genistein and resveratrol protect rodents against che
mically induced and spontaneous
ma
mmary cancers. This is reported to occur through the ability of genistein and resveratrol to accelerate
ma
mmary gland
maturation. Interestingly, TCDD, which is the
most structurally dissi
milar to the above che
micals and functions as an anti-estrogen, also increases che
mically induced
ma
mmary carcinogenesis through retardation of
ma
mmary gland
maturation.
This article is part of a Special Issue entitled 鈥楨ndocrine disruptors鈥?