The natural hormone 17beta-estradiol (E2) is considered an endogenous cancer risk factor, and one possible mechanism of carcinogenesis involving E2 is through the induction of oxidative stress. E2 is metabolized to two catecholestrogens, 2-OHE2 and 4-OHE2, by CYP1A1 and CYP1B1, respectively. Both metabolites can contribute to metabolic redox cycling, which induces ROS and causes the formation of 8-hydroxy-2'-deoxyguanosine (8-OH-dG). Since the levels of E2 change in accordance with the menstrual cycle in women, it is important to consider the menstrual cycle when assessing the risk posed to female workers when they are exposed to substances inducing ROS. In the present study, we investigated whether the levels of urinary 8-OH-dG changed during the different phases of the menstrual cycle. The test subjects were all female office workers from the same company. Information on demographic factors, phases of the menstrual cycle , and lifestyle factors were obtained from self-administered questionnaires which were then checked during interviews. Urine specimens were collected in the morning and were used to measure 8-OH-dG, E2, and creatinine levels. The concentrations of 8-OH-dG and E2 were normalized against creatinine content. The test subjects who provided menstrual cycle information (non-smokers who did not take hormone-like medicines) were classified into four groups, depending whether they were in their menstrual phase (n=15), follicular phase (n=35), luteal phase (n=28), or in menopause (n=15). Although the difference was not statistically significant, the urinary 8-OH-dG level of the luteal phase group was higher than that of the menstrual phase group (4.1±0.6 μg/g creatinine and 3.0±0.4μg/g creatinine, respectively). These results suggested that the level of the oxidative state during the luteal phase was higher than that during the menstrual phase.
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