Abstract
Reduction of circulating melatonin levels by pinealectomy or constant light has previously been shown to enhance the development and growth of mammary cancers induced by the polyaromatic hydrocarbon 7,12-dimethylbenz[a]anthracene (DMBA) in female rats. Since pineal melatonin production can also be disturbed by electromagnetic field exposure, we studied whether there is an association between melatonin depression by magnetic field (MF) exposure and DMBA-induced breast cancer growth in female rats. In the present experiments, 216 female Sprague-Dawley rats were divided into 4 groups. Two of the groups (with 99 animals each) received oral applications of DMBA and were either sham-exposed or exposed in a 50-Hz, 100-mG (10 microT) MF for 24 h/d, 7 d/wk, for a period of 91 d. 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. The animals were palpated once weekly to assess the development of mammary tumors. At the end of the exposure period, all animals were sacrificed for autopsy and determination of nocturnal melatonin levels in pineal and serum. In controls, DMBA induced palpable tumors in about 55% of the animals within 3 mo after first application. There was a tendency to an enhanced tumor incidence in MF-exposed rats throughout the period of exposure, which, however, was not statistically significant. At autopsy, 60.6% of the sham-exposed and 66.6% of the MF-exposed rats had developed macroscopically visible mammary tumors. Tumor size and tumor burden were similar in both groups. Compared to the groups without DMBA treatment, DMBA-treated rats had significantly lower nocturnal pineal melatonin levels without difference in terms of MF exposure. MF-exposed rats, however, had significantly lower nocturnal melatonin levels in serum than sham-exposed animals. The data demonstrate that although exposure of female rats to a 50-Hz, 100-mG MF significantly decreases circulating melatonin, this is not associated with a significant effect on development or growth of DMBA-induced mammary tumors. In view of the fact that, by using the same model, we recently demonstrated a tumor-copromoting effect of MF exposure at a 10 times higher flux density, the effects of MF exposure on DMBA-induced mammary carcinogenesis appear to be dose dependent.
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