Baum A, Mevissen M, Kamino K, Mohr U, Löscher W
Institute of Experimental Pathology, Medical School Hannover, Germany.
Carcinogenesis. 1995 Jan;16(1):119-25. doi: 10.1093/carcin/16.1.119.
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 methodological problems of epidemiological studies on MF exposure and cancer risk, laboratory studies are needed to determine whether 50/60 Hz exposure can initiate, promote or copromote 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 applications of 7,12-dimethylbenz[a]anthracene (DMBA) and were either sham-exposed or exposed in a 50 Hz, 100 muT MF for 24 h/day 7 days/week for a period of 91 days. The other two groups (nine animals each) were either sham-exposed or MF-exposed without DMBA treatment. The exposure chambers and all other environmental factors were identical for MF-exposed and sham-exposed animals. At the end of the 3 month period of MF 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 MF 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 MF 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 MF 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.
多项流行病学研究表明，居住或职业性接触50或60赫兹的磁场（MF）可能会增加患乳腺癌的风险，这可能是通过抑制松果体产生抑癌激素褪黑素实现的。鉴于关于MF暴露与癌症风险的流行病学研究存在方法学问题，需要进行实验室研究来确定50/60赫兹的暴露是否会引发、促进或协同促进乳腺癌。在本研究中，将216只雌性斯普拉格-道利大鼠分为四组。其中两组（每组99只动物）口服7,12-二甲基苯并[a]蒽（DMBA），并分别接受假暴露或在50赫兹、100微特斯拉的MF中暴露，每天24小时，每周7天，持续91天。另外两组（每组9只动物）分别接受假暴露或MF暴露，但不进行DMBA处理。暴露室和所有其他环境因素对于MF暴露组和假暴露组动物是相同的。在MF暴露3个月结束时，所有大鼠均用于病变的组织病理学诊断。在尸检时，与接受DMBA处理的对照组相比，接受MF暴露且经DMBA处理的大鼠中，肉眼可见的乳腺肿瘤明显更多。此外，MF暴露组大鼠的乳腺肿瘤尺寸明显更大。乳腺组织病理学检查表明，各组之间肿瘤性和非肿瘤性病变的数量没有显著差异，这表明MF暴露并未改变乳腺病变的发生率，而只是加速了肿瘤生长，这与协同促进作用一致。在MF暴露组中，出现恶性乳腺肿瘤的大鼠明显多于对照组，这表明MF暴露影响了DMBA诱导病变的进展。MF暴露对DMBA诱导的乳腺肿瘤转移或其他器官原发性病变的数量没有影响。在未应用DMBA的大鼠中，未发现非肿瘤性或肿瘤性病变。数据表明，长期暴露于经DMBA处理的雌性大鼠会促进乳腺肿瘤的生长和进展，而肿瘤发生率不受影响，至少在本研究的实验条件下如此。这些数据因此进一步证明了MF暴露具有肿瘤协同促进作用。
