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© 1995 Oxford University Press
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A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with 50 Hz, 100 µT magnetic field exposure
Institute of Experimental Pathology, Medical School Hannover Hannover, Germany
1Department of Pharmacology, Toxicology and Pharmacy, School of Vetennary Medicine Hannover, Germany
2To whom correspondence should be addressed
Several epidemiological studies have indicated that residential or occupational exposure to 50 or 60 Hz magnetic fields (MF) may increase the risk of breast cancer, possibly by suppression of pineal production of the oncostatic hormone melatonin. In view of the methodo logical problems of epidemiological studies on MIF exposure and cancer risk, laboratory studies are needed to determine whether 50/60 Hi exposure can initiate, promote or co promote mammary cancer. In the present study, 216 female Sprague-Dawley rats were divided into four groups. Two of the groups (with 99 animals each) received oral applica tions of 7,12-dimethylbenz (DMBA) and were either sham-exposed or exposed in a 50 Hz, 100 µT ME for 24 h/day 7 days/week for a period of 91 days. The other two groups (nine animals each) were either shamexposed or MF-exposed without DMBA treatment. The exposure chambers and all other environmental factors were identical for ME-exposed and sham-exposed animals. At the end of the 3 month period of ME exposure, all rats were used for histopathological diagnosis of lesions. At the time of necropsy, significantly more MF-exposed DMBA-treated rats exhibited macroscopically visible mammary tumours than DMBA-treated controls. Furthermore, the size of mammary tumours was significantly larger in MF-exposed rats. Histopathological examination of the mammary gland showed that the number of neoplastic and non-neoplastic lesions did not significantly differ between groups, indicating that ME exposure had not altered the incidence of mammary lesions but had only accelerated tumour growth, consistent with a co-promoting effect. In the MF-exposed group, significantly more rats exhibited malignant mammary tumours than in controls, indicating that ME exposure had affected the progression of DMBA Induced lesions. The number of metastases of mammary tumours or of primary lesions in other organs in response to DMBA was not affected by ME exposure. In rats without DMBA application, no non-neoplastic or neoplastic lesions were determined. The data demonstrate that long-term exposure of DMBA-treated female rats promotes the growth and progression of mammary tumours, while tumour incidence is not affected, at least under the experimental conditions of the present study. The data thus add to the accumulating evidence that MF exposure exerts tumour co-promoting effects.
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