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Last Updated: 2 years ago

Possible Interaction: Estradiol and Indole-3-Carbinol

Research Papers that Mention the Interaction

Indole-3-carbinol affects the ratio of hydroxylation of estradiol ; changes in the ratios of urinary 2-hydroxylation and 16-hydroxylation of estradiol caused by indole-3-carbinol correlated well with clinical response.
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery  •  1998  |  View Paper
Additionally, I3C can reduce cervical dysplasia caused by estradiol in the normal mouse (3).
The Journal of nutrition  •  2006  |  View Paper
Estradiol reduced the percentage of these late-stage apoptotic cells in the cervical epithelium of transgenic, E2-treated mice, but this reduction was prevented by I3C.
The Journal of nutrition  •  2001  |  View Paper
b. Diminishing the capacity to 16 α-hydroxylate estradiol , either through pharmacological agents such as indole-3-carbinol or through increased consumption of cruciferous vegetables.
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine  •  1998  |  View Paper
The suggestion that ICZ can inhibit estrogen activity via induction of the cytochrome P450 monoxygenase system comes from studies showing that TCDD and I3C increase CYPlA2-catalyzed 2hydroxylation of estradiol and, as a consequence, decrease the estrogen response (7).
Journal of the National Cancer Institute  •  1994  |  View Paper
Indole-3-carbinol , which induces 2-hydroxylation, abrogated the proliferative effects of estradiol.
Anticancer research  •  1993  |  View Paper
This inhibition was partially reversed by the addition of indole-3-carbinol , a potent inducer of 2-hydroxylation of estradiol.
In vivo  •  2011  |  View Paper
I3C inhibited 17β-estradiol stimulated hTERT expression and stimulated the production of threonine-phosphorylated Sp1, which inhibits Sp1-DNA interactions.
Carcinogenesis  •  2011  |  View Paper
Higher concentrations of I3C overcame the anti-apoptotic effect of estradiol.
Protection was independent of HPV gene expression, and not specific to apoptosis induced by DNA damage, since estradiol significantly reduced the number of apoptotic cells produced after exposure to indole-3-carbinol (I3C), a non-genotoxic phytochemical effective in preventing HPV-induced tumors.
Treatment with I3C resulted in loss of the survival protein Bcl-2, and estradiol partially reversed this effect.
Anticancer research  •  2004  |  View Paper
I3C abrogates the cell-proliferative effect of 17β-estradiol (E2), as observed in several different estradiol-responsive breast cancer cell lines and isolated cell clones.
Nutrition and cancer  •  2001  |  View Paper
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