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Title: STUDIES ON RADIATION-INDUCED MAMMARY GLAND NEOPLASIA IN THE RAT. VI. THE EFFECT OF CHANGES IN THYROID FUNCTION, OVARIAN FUNCTION, AND PREGNANCY

Journal Article · · Radiation Res.
DOI:https://doi.org/10.2307/3571175· OSTI ID:4780360

When 3l female Sprague-Dawley rats were exposed to a single total-body dose of 400 r of 250 kvp x rays on the fortieth day of age, 24 of the rats so exposed developed 43 mammary neoplasms within a 1-year period. Of 3l littermate control rats studied during the same period, only 3 rats exhibited single mammary neoplasms. When diethylstilbestrol was given to irradiated rats, both the incidence and the number of mammary neoplasms was depressed, indicating that for the maximum mammary neoplastic response to radiation the irradiation breast tissue must be subjected to the proper hormonal environment, and this appears to be provided by a normal estrus cycle. Diethylstilbestrol given to nonexposed rats did not induce any more mammary neoplasms than were found in nonexposed control rats. Hyperthyroidism, induced by exogenous triiodothyronine given after irradiation and maintained for 12 months, did not infiuence the incidence of rats with mammary neoplasia or the total number of mammary neoplasms. Hypothyroidism, induced by a continuous administration of propylthiouracil in the drinking water beginning after irradiations, reduced the incidence of rats with mammary neoplasia only slightly and further reduced the total number of mammary neoplasms, suggesting that hypothyroidism provides less than the optimum hormonal pattern for the maximum mammary neoplastic response to radiation exposure. When the ovarian area was shielded, including a portion of mammary tissue, the incidence and number of mammary neoplasms were reduced. This reduction of neoplastic response appears to be due to the fact that, as less breast tissue is exposed, the smaller the total neoplastic response becomes. When 30 rats were irradiated with the ovarian area shielded and then allowed to become pregnant (with and without lactation), 19 of these rats exhibited 29 mammary neoplasms. This slight increase in neoplastic response was not proved to be significant, although it is suggestive that the changes in hormonal patterns brought about by pregnancy may also influence the neoplastic potential of irradiated breast tissue. Immediately after parturition, with or without lactation permitted, the growth rate of the adenocarcinoma type of mammary neoplasm was diminished, suggesting that in this type of mammary neoplasm the growth rate may be hormone-dependent, a conclusion reached previously by others. Twenty-nine per cent of the mammary neoplasms found in the irradiated groups were of the adenocarcinoma type; no adenocarcinomas were found in non-irradiated rats. Neoplasms of the adenofibroma or fibroadenoma types were the most common types found in either exposed or nonexposed animals. The period between exposure and appearanee of the first mammary neoplasm was 2 months in all irradiated groups. The comparable period for the nonirradiated was 12 months. Thus the irradiated female Sprague-Dawley rat develops a relatively high incidence of rapidly appearing mammary neoplasms as compared to nonirradiated rats, although the mammary neoplastic response to irradiation is subject to hormonal modification. This suggests that radiation- induced neoplasia, of this type in this strain of rat, is at least a two-stage proccss consisting of the induction phase, i.e., radiation injury, and thc promoting phase, i.e., the hormonal influence to which the radiation injured tissue is subjected. The total incidence of neoplasia of the pituitary, thyroid, and adrenal glands and of the ovaries did not exceed 6% in the exposed animals, as compared to an absence of these neoplasms in the nonexposed animals. The numbers of these neoplasms were ioo small to permit meaningful conclusions to be drawn as to the effects of changes in thyroid function, ovarian function, or pregnancy and lactation superimposed on radiation exposure on neoplasia of the endocrine system. (auth)

Research Organization:
Brookhaven National Lab., Upton, N.Y.
NSA Number:
NSA-16-032791
OSTI ID:
4780360
Report Number(s):
BNL-5825
Journal Information:
Radiation Res., Vol. Vol: 17; Other Information: BNL-5825. Orig. Receipt Date: 31-DEC-62
Country of Publication:
United States
Language:
English