Figure 1.
Current three (A, B & C) major hypotheses that have been proposed for estrogen induced carcinogenicity.
D-Newly proposed pathway of estrogen metabolism that could initiate cancer in human.
Table 1.
Average levels of steroids in breast tissue of healthy women.a.
Figure 2.
Estrogens were oxidized by chemical means as described in Materials and method.
UV spectra and plot presenting decay of estrone quinone methide (E1QM) (A) and estradiol quinone methide (E2QM) (B). Observed t 1/2 for E1QM and E2QM was 20.8 and 4.5 min respectively.
Figure 3.
MS/MS spectra of E1QM (A) and E2QM (B).
A plausible fragmentation of parent ions (269 and 271, M+1 ions) leading to major peaks is presented.
Figure 4.
UPLC–MS/MS chromatogram of assay mixture (A) and standard E1-9-N-Ade (B).
E1-9-N-Ade was formed by peroxidase-catalyzed oxidation of E1 through methide. Insets: MS/MS spectra of E1-9-N-Ade from assay mixture (A) and standard E1-9-N-Ade (B). A plausible fragmentation of parent ion (404, M+1 ion) leading to major peaks is presented. Arrows indicate peaks that are common to assay mixture and standard.
Figure 5.
UPLC–MS/MS chromatogram of assay mixture (A) and standard E2-9-N-Ade (B).
E2-9-N-Ade was formed by peroxidase-catalyzed oxidation of E2 through methide. Insets: MS/MS spectra of E2-9-N-Ade from assay mixture and standard E2-9-N-Ade. A plausible fragmentation of parent ion (406, M+1 ion) leading to major peaks is presented. Arrows indicate peaks that are common to standard and assay mixture.
Figure 6.
Breast tissue samples were homogenized and extracted as described in Materials and Methods.
UPLC–MS/MS chromatogram of standard E1(E2)-9-N-Ade (A, C) and breast tissue extract (B, D).