Skip to main content
. Author manuscript; available in PMC: 2016 Nov 1.
Published in final edited form as: Trends Cancer. 2015 Nov 1;1(3):174–182. doi: 10.1016/j.trecan.2015.08.011

Figure 3.

Figure 3

Schematic representation to explain the appearance DNA adducts recovered from schistosomes or liver flukes and helminth-infected people. In steroidogenesis, cholesterol is the protypical animal setrol precursor for estradiol, the primary female sex hormone. Also, oxysterols are oxidation products of cholesterol. Structures A, D and E depict estradiol (A), cholesterol (D), and 4β-hydroxycholesterol, an oxysterol (E). Examples of potentially reactive catechol estrogen quinones are shown in B. Structure C presents examples of catechol estrogen quinone-DNA adducts from urine during urogenital schistosomiasis [48, 59]. Hydroxylation of estrogens forms the 2- and 4-catechol estrogens, which can be further oxidized to semiquinones and quinones, including the catechol estrogen-3,4-quinones, the major carcinogenic metabolites of estrogens [53]. These kinds of electrophiles can react with DNA to produce depurinating adducts such as those shown n panel E that, in turn, can lead to mutations and cancer initiation [53].