| Popis: |
Prolonged, uncontrolled treatment with oestrogens or excessive endogenous production over a long period can lead to the development of pathological processes, including neoplastic growth. We proposed earlier that there are two principal types of hormonal carcinogenesis and suggested that there are factors that facilitate a shift from promotional (mitogenic) to genotoxic types (Berstein, 1996a). We consider that tobacco smoking is an important exogenous factor which can modify both the frequency of some malignant tumours and endocrine function (Peto et al., 1992). Women who smoke cigarettes are at increased risk not only of lung cancer but also of osteoporosis and early menopause; decreased risks for endometrial cancer, endometriosis and uterine fibroids have been reported. Although it has been assumed that the mechanism of these decreases is hypo-oestrogenism (Wald & Baron, 1990), that conclusion is not supported by direct studies of blood oestrogen concentrations in smokers. The change in oestrogen production in smokers may be mainly qualitative, with a shift to the powerful genotixicant catechol oestrogens (Liehr & Ricci, 1996), thus reducing the total oestrogenic effect. On the basis of these observations, we assumed that tobacco smoke weakens the specific effect of oestrogens but augments their capacity to damage DNA (Berstein, 1996a; Berstein et al., 1997). The aim of the study reported here was to verify this hypothesis experimentally. |
