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PubMed1956

Effects of hormones on the adrenal necrosis produced by Besnoitia jellisoni in golden hamsters.

Adrenal necrosis has been described in golden hamsters where it occurs during the course of infection with Besnoilia jellisoni. This necrosis results directly from the active intracellular proliferation by this obligate intracellular protozoan organism. After infection, adrenal necrosis is rarely observed in hypophysectomized hamsters. In unoperated animals adrenal necrosis is suppressed to varying degrees by cortisone (E), hydrocortisone (F), corticosterone (B), 11-dehydrocorticosterone (A), and possibly by 11-desoxycorticosterone (DOCA). Besnoitia organisms proliferate in otherwise "immune" hamsters around the subcutaneous deposits of the acetates of cortisone (E), hydrocortisone (F), and 11-dehydrocorticosterone (A); a marked depression of general immunity follows the administration of pharmacologic doses of the former two hormones. Organisms do not proliferate around the sites of corticosterone acetate (B) and 11desoxycorticosterone acetate (DOCA) injection, nor next to deposits of testosterone propionate, 11-desoxy-17-hydroxycorticosterone acetate (Reichstein's compound S) and epinephrine in oil. It is postulated that certain glucocorticoids can so modify immunity mechanisms locally, that general immunity becomes ineffective; this occurs in the adrenal glands owing to endogenous corticoid production, at the sites of exogenous corticoid injection, and proximal to that in the lungs. A comparison is made with the pathogenesis of tuberculosis and histoplasmosis of the adrenal gland which results in Addison's disease in man, and it is concluded that a similar pathogenetic mechanism is operative. The use of glucocorticoids for replacement therapy is discussed in reference to their relative resistance-depressing activities in pharmacologic doses. These undesirable side effects would appear to be less pronounced, if not absent, if corticosterone (B) rather than cortisone (E) and hydrocortisone (F) therapy were used. Porcine adrenocorticotrophic hormone (ACTH) appearsto depress the incidence of adrenal necrosis in unoperated hamsters, and supports proliferation of organisms in the adrenal cortex with subsequent necrosis in only a small proportion of hypophysectomized hamsters. The possibility is discussed that ACTH from a different species (hog) might lead to a change in the secretory activity of the hamster adrenal gland.

Adrenal Gland Diseases↗
PubMed1956

Hormonal influences on mammary tumors of the rat. I. Acceleration of growth of transplanted fibroadenoma in ovariectomized and hypophysectomized rats.

A transplanted mammary fibroadenoma was found to grow in 95 per cent of intact adult female rats and the increment of tumor weights was progressive and logarithmic. The growth of the tumor was retarded by ovariectomy and still more when this was combined with adrenalectomy. In ovariectomized rats the growth of the tumor was stimulated by phenolic estrogens, this increase being enhanced when progesterone was added. In these responses to hormonal changes the mammary gland and the tumor resembled each other. Yet there are many differences between the growth of the fibroadenoma and that of the mammary gland. In contrast to the progressive growth which occurred in intact adult females there was a prolonged period of indolent growth of transplants in hypophysectomized rats; but after many weeks active growth began and the tumors eventually reached large size. During the period of quiescent growth the tumor was cytologically atrophic but after the growth spurt had started the microscopic appearance of the fibroadenoma resembled that of tumors growing in normal adult females. The mammary gland remained atrophic during both the slow and the accelerated phases of tumor growth, and so too with the other secondary sex expressions. In hypophysectomized rats estrone and progesterone, when combined, stimulated the growth of the tumor, and this growth was accelerated by the additional administration of lactogenic or growth hormones. None of these hormones, separately, stimulated the growth of the tumor. In ovariectomized rats other differences were demonstrated between the growth of the mammary gland and the fibroadenoma. Progesterone, injected alone, accelerated the growth of the tumor but not that of the mammary glands. The administration of phenolic estrogens exerted a biphasic effect on the growth of the tumor whilst that on the breast of its hosts was monophasic. With progressively increasing doses of these phenols there occurred primarily an augmentation of the rate of growth of the tumor until a peak was achieved; an increase of the dose above the optimal amount depressed the growth of the tumor. The stage of depression of growth was not observed in the mammary glands of these tumor-bearing rats. Many steroids which induced gestational changes in the mammary gland accelerated the growth of the tumor. Among these were estrone and progesterone in combination and 17alpha-ethinyl-19-nor-testosterone administered alone. But gestational changes developed in the mammary gland of rats treated with 4-androstene-3alpha,17beta-diol, without growth of the tumor. The evidence which we have presented proves that the mammary fibroadenoma tested had some of the functional properties of a normal mammary gland, and neoplastic traits as well. In its response to hormones it had characteristics which set it apart from all other endocrine targets of the rat.

Adenofibroma↗
PubMed1959

Rapid induction of mammary carcinoma in the rat and the influence of hormones on the tumors.

A study was made of the optimal conditions for the induction of mammary cancer in the rat. 3-Methylcholanthrene was administered via the gastrointestinal tract, and a simple technique was worked out for inducing mammary cancer regularly and rapidly. Under conducive conditions, which were readily reproduced, multiple mammary carcinomas and these tumors only were induced in every rat in repeated experiments in 60 days or less. In the strain of animal employed in the present experiments, the rapid induction of mammary cancer proved to be a function of (a) dosage, (b) the timing of administration of the aromatic hydrocarbon, and (c) a favoring hormonal status of the recipient. Most of the established tumors were hormone-dependent because they diminished markedly in size after hormone withdrawal through ovariectomy or hypophysectomy. Similar regression of the tumors was frequently achieved by the administration of dihydrotestosterone. Shrinkage of the cancers was accompanied by atrophic changes. Experimental mammary tumors with these physiologic characteristics have not been recognized hitherto. The minority of mammary cancers continued to grow after ovariectomy; these are hormone-independent tumors and tumors of this sort had a characteristic cytologic appearance following modification of the endocrine state. The cell population of a single tumor was not always uniform in its response to appropriate hormonal modifications. In certain tumors in response to changes in the endocrine status of the host many of the cells underwent atrophy whilst other adjacent cells in the same tumor continued to grow so that the net result was a hormone-independent tumor. Hypophysectomy was the most effective method found to induce regression of mammary cancer in the present experiments.

Animals↗