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Author |
Loscher, W.; Mevissen, M. |
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Title |
Animal studies on the role of 50/60-Hertz magnetic fields in carcinogenesis |
Type |
Journal Article |
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Year |
1994 |
Publication |
Life Sciences |
Abbreviated Journal |
Life Sci |
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Volume |
54 |
Issue |
21 |
Pages |
1531-1543 |
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Keywords |
Animals; Environmental Exposure; Female; Humans; Incidence; Magnetics/*adverse effects; Male; Mice; Neoplasms/*epidemiology; Neoplasms, Experimental/etiology/*physiopathology; Rats |
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Abstract |
A number of epidemiological studies have suggested that exposure to 50/60-Hz magnetic fields (MF) from power lines and electrical equipment may be associated with a modestly increased incidence of various types of cancer. Laboratory studies have indicated that nonionizing radiation has no mutagenic effect, i.e. does not initiate cancer. Thus, if 50/60-Hz MF are truly associated with an increased risk of cancer, then these fields must act as a promoter or co-promoter of cancer in cells that have already been initiated. This paper reviews the evidence produced by animal studies. As shown in this review, the available animal data on 50/60-Hz MF exposures seem to indicate that intermediate MF exposure exerts co-promoting effects in different tumor models, particularly cocarcinogenesis models of breast cancer, while chronic (up to life-time) exposure may exert promoting effects on “spontaneous” development of certain tumors. The tumor promoting or co-promoting effects of 50/60-Hz MF exposure found in several animal studies could relate to actions of MF on gene expression, immune surveillance, and Ca2+ homeostasis as demonstrated by in vitro experiments in cell cultures. However, the most plausible evidence for an in vivo effect of MF exposure which could be related to tumor promotion is reduction of circulating levels of melatonin, i.e. a hormone which is inhibitory to the growth of a wide range of cancers, particularly breast cancer. Animal studies have shown that 50-Hz MF exposure at flux densities as low as 0.3-1 mu Tesla significantly reduces nocturnal melatonin levels in plasma. While decrease of melatonin levels alone could explain tumor promoting or co-promoting effects of MF exposure, recent data indicate that MF exposure also impairs the effects of melatonin at the cellular level. Thus, the oncostatic effect of melatonin on cell proliferation of a human breast cancer cell line was antagonized by 60-Hz MF exposure at a flux density of about 1 mu Tesla. All these data indicate that interactions between 50/60-HZ MF exposure and melatonin may be the key mechanism of any carcinogenic effects. Although the existing experimental evidence is still insufficient for discerning a cause-effect relationship for MF exposure and human disease or injury, it does suggest the need for further laboratory research under well-defined laboratory exposure conditions to allow for a realistic assessment of the possible health risks and their magnitude. |
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Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Hannover, Germany |
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ISSN |
0024-3205 |
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WP6 In vivo |
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Notes |
PMID:8196474 |
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Call Number |
ITEM @ geertje.lewin @ |
Serial |
137 |
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Author |
Mevissen, M.; Buntenkotter, S.; Loscher, W. |
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Title |
Effects of static and time-varying (50-Hz) magnetic fields on reproduction and fetal development in rats |
Type |
Journal Article |
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Year |
1994 |
Publication |
Teratology |
Abbreviated Journal |
Teratology |
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Volume |
50 |
Issue |
3 |
Pages |
229-237 |
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Keywords |
Animals; *Embryonic and Fetal Development; Female; *Magnetics; Male; Pregnancy; Rats; Rats, Wistar; *Reproduction; Time Factors |
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Abstract |
Mated Wistar rats were chronically exposed to a static magnetic field (MF) from day 1 to day 20 of pregnancy. Flux density of the MF was 30 mTesla (mT), i.e., within the range of exposures of operators of magnetic resonance imaging (MRI) devices. For comparison with effects of this static field, a time-varying (50-Hz) MF of the same flux density was used. In both experiments, i.e., static or 50-Hz MF exposure, sham-exposed groups of dams served as controls. On day 20, the dams were sacrificed for reproductive and teratological assessment. The litters were evaluated for numbers of implantations, fetal deaths and resorptions, gross external, visceral, and skeletal malformations, and fetal weights. No adverse effects were seen in the dams during MF exposure. The mean number of living fetuses per litter was significantly decreased in the group with static MF exposure, but not the group with 50-Hz MF exposure. Further differences between the two types of field exposure were observed with respect to minor (skeletal) fetal anomalies which were increased in the 50-Hz but not the static MF group. No serious malformations were seen in any group. In both MF-exposed groups, increased skeletal ossification was found, possibly indicating an accelerated prenatal development. In a second experiment with static MF (30 mT) in which dams were exposed for the whole period of pregnancy, and postnatal growth and development of offspring were studied, the postnatal growth was significantly enhanced in offspring following their prenatal MF exposure.(ABSTRACT TRUNCATED AT 250 WORDS) |
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Department of Pharmacology, Toxicology, and Pharmacy, School of Veterinary Medicine, Hannover, Germany |
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ISSN |
0040-3709 |
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WP6 In vivo |
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Notes |
PMID:7871487 |
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Call Number |
ITEM @ geertje.lewin @ |
Serial |
136 |
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Author |
Baum, A.; Mevissen, M.; Kamino, K.; Mohr, U.; Loscher, W. |
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Title |
A histopathological study on alterations in DMBA-induced mammary carcinogenesis in rats with 50 Hz, 100 muT magnetic field exposure |
Type |
Journal Article |
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Year |
1995 |
Publication |
Carcinogenesis |
Abbreviated Journal |
Carcinogenesis |
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Volume |
16 |
Issue |
1 |
Pages |
119-125 |
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Keywords |
*9,10-Dimethyl-1,2-benzanthracene; Animals; Behavior, Animal/drug effects; *Cocarcinogenesis; Electromagnetic Fields/*adverse effects; Female; Hyperplasia/chemically induced/etiology; Magnetics/*adverse effects; Mammary Glands, Animal/drug effects/pathology; Mammary Neoplasms, Experimental/chemically induced/*etiology/*pathology; Methylnitrosourea; Rats; Rats, Sprague-Dawley |
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Abstract |
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. |
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Institute of Experimental Pathology, Medical School Hannover, Germany |
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ISSN |
0143-3334 |
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WP6 In vivo |
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Notes |
PMID:7834796 |
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Call Number |
ITEM @ geertje.lewin @ |
Serial |
141 |
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Author |
Dhabhar, F.S.; Miller, A.H.; McEwen, B.S.; Spencer, R.L. |
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Title |
Differential activation of adrenal steroid receptors in neural and immune tissues of Sprague Dawley, Fischer 344, and Lewis rats |
Type |
Journal Article |
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Year |
1995 |
Publication |
Journal of Neuroimmunology |
Abbreviated Journal |
J Neuroimmunol |
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Volume |
56 |
Issue |
1 |
Pages |
77-90 |
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Keywords |
Adrenal Glands/*metabolism; Adrenocorticotropic Hormone/blood; Animals; Corticosterone/blood; Immune System/*metabolism; Male; Nerve Tissue/*immunology; Rats; Rats, Inbred F344; Rats, Inbred Lew; Rats, Inbred Strains; Rats, Sprague-Dawley; Receptors, Glucocorticoid/metabolism; Receptors, Mineralocorticoid/metabolism; Receptors, Steroid/*metabolism; Species Specificity; Transcortin/metabolism |
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Abstract |
Sprague Dawley (SD), Fischer 344 (F344), and Lewis (LEW) rats are used in a wide variety of laboratory studies. Compared to SD and LEW rats, F344 rats show significantly greater corticosterone secretion in response to stress, or to immune challenge. These strain differences in hypothalamic-pituitary-adrenal (HPA) axis responsivity have been the basis for many comparative studies investigating immunological and behavioural differences between the three strains. However, the effects of these strain differences in HPA axis responsivity have not been investigated at the level of adrenal steroid receptor activation in target tissues. The present study demonstrates that compared to SD and LEW rats, F344 rats exhibited a greater magnitude of Type II adrenal steroid receptor activation in brain tissues during stress. In contrast, Type II receptor activation in immune tissues of F344 rats following stress was similar to that of SD rats. Importantly, LEW rats exhibited the lowest magnitude of activation of Type II receptors in immune tissues during stress. No differences were observed between strains in the extent of stress-induced Type I adrenal steroid receptor activation. The observed differences between strains in corticosteroid-binding globulin (CBG) levels in plasma, pituitary, and immune tissue may mediate the differential access of corticosterone to neural versus immune tissues. These results indicate that strain differences in corticosterone secretion are manifested by differences in Type II receptor activation in neural as well as immune tissues. Moreover, they suggest that increased access of corticosterone to adrenal steroid receptors in brain areas of F344 rats may contribute to behavioural differences between strains, whereas decreased access of hormone to receptors in immune tissues of LEW rats may contribute to strain differences in susceptibility to autoimmune disease. |
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Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021 |
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ISSN |
0165-5728 |
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WP6 In vivo |
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PMID:7822484 |
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Call Number |
TIHO @ Maren.Fedrowitz @ |
Serial |
116 |
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Author |
Uckun, F.M.; Kurosaki, T.; Jin, J.; Jun, X.; Morgan, A.; Takata, M.; Bolen, J.; Luben, R. |
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Title |
Exposure of B-lineage lymphoid cells to low energy electromagnetic fields stimulates Lyn kinase |
Type |
Journal Article |
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Year |
1995 |
Publication |
The Journal of Biological Chemistry |
Abbreviated Journal |
J Biol Chem |
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Volume |
270 |
Issue |
46 |
Pages |
27666-27670 |
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Keywords |
Amino Acid Sequence; B-Lymphocytes/enzymology/*radiation effects; Benzoquinones; Cell Line; *Electromagnetic Fields; Enzyme Inhibitors/pharmacology; Enzyme Precursors/deficiency; Genistein; Humans; Intracellular Signaling Peptides and Proteins; Isoflavones/pharmacology; Lactams, Macrocyclic; Molecular Sequence Data; Myelin Basic Protein/metabolism; Peptide Fragments/chemistry/metabolism; Phosphoproteins/isolation & purification/metabolism; Phosphotyrosine/analysis; Protein Kinase C/metabolism; Protein-Tyrosine Kinases/antagonists & inhibitors/deficiency/*metabolism/radiation effects; Quinones/pharmacology |
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Abstract |
Here, we present evidence that exposure of B-lineage lymphoid cells to low energy electromagnetic fields (EMF) stimulates the protein tyrosine kinases Lyn and Syk, results in tyrosine phosphorylation of multiple electrophoretically distinct substrates, and leads to downstream activation of protein kinase C (PKC). EMF exposure enhances protein tyrosine phosphorylation in Syk deficient but not in Lyn-deficient B-lineage lymphoid cells and stimulates Lyn kinase activity in wild-type as well as Syk-deficient B-lineage lymphoid cells. These results indicate that activation of Lyn kinase is sufficient and mandatory for EMF-induced tyrosine phosphorylation in B-lineage lymphoid cells. The PKC activity increases later than the Lyn activity and pretreatment with the PTK inhibitors genistein or herbimycin A abrogates the EMF-induced PKC signal. Thus, stimulation of Lyn is a proximal and mandatory step in EMF-induced activation of PKC in B-lineage lymphoid cells. Our observations prompt the hypothesis that a delicate growth regulatory balance might be altered in B-lineage lymphoid cells by EMF-induced activation of Lyn. |
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Department of Therapeutic Radiology-Radiation Oncology, University of Minnesota Health Sciences Center, Minneapolis 55455, USA |
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0021-9258 |
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PMID:7499232 |
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Call Number |
IT'IS @ evaj @ |
Serial |
424 |
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