Abstract
The thymus gland of rats can be made to regress rapidly by the administration of extracts of the adrenal cortex or by the administration of some of the steroid compounds occurring in the extracts. In studies of the biologic effects of 11-desoxy-corticosterone acetate and 17-hydroxy-11-dehydro-corticosterone acetate it was noted that the latter substance was the more active of the two in producing thymus atrophy.
Male rats of the Sprague-Dawley strain each having an initial body-weight of approximately 180 g were used. The diet was Purina Dog Chow. The test substances were dissolved in sesame oil and administered twice daily by subcutaneous injection. Ten normal rats were killed in order to obtain control data on thymus weights; 10 adrenalectomized rats were maintained for 7 days without treatment; 5 adrenalectomized rats were treated with 2 mg daily of 17-hydroxy-11-dehydro-corticosterone acetate; 5 adrenalectomized rats were treated with 2 mg of 11-desoxy-corticosterone; and 5 adrenalectomized rats were treated with 10.0 mg daily of 11-desoxy-corticosterone. Necropsy was performed on the 7th day. The data on body weights and thymus weights are summarized in Table I.
Although 2 mg daily of 17-hydroxy-11-dehydro-corticosterone acetate did not protect the adrenalectomized rat against a loss in body weight it did produce a marked regression of the thymus. A similar dose of 11-desoxy-corticosterone acetate permitted the adrenalectomized rat to gain in weight during the period of treatment but it did not produce a significant regression of the thymus. The administration of 10 mg daily of 11-desoxy-corticosterone acetate did produce a definite loss in thymus weight but the extent of atrophy was much less than that produced by the 2.0 mg daily dose of 17-hydroxy-11-dehydro-corticosterone acetate. Selye 1 has previously observed a regression of the thymus following the administration of 11-desoxy-corticosterone to rats.
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