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Chronic hyperthyroidism was induced in radiothyroidectomized and surgically thyroidectomized adult male rats by feeding a diet of 0 3 4 . 4 % desiccated thyroid for four to ten week periods. Short term hyperthyroidism was induced in intact rats by the intraperitoneal injection of 250 pg/day of sodium levothyroxine for ten days. Adrenal glands were fixed by perfusion with 3% phosphate buffered glutaraldehyde and post-fixed in 1 % osmium tetroxide. The zona fasciculata of the adrenal glands from experimental and control animals was examined in the electron microscope. Drastic mitochondrial alterations characterized the zona fasciculata of hyperthyroid rats. Initially, mitochondria became more nearly round and contained increased numbers of paracrystalline tubular inclusions of the type described by Kjaerheim ('67) and Wheatley ('68).In more altered states many mitochondria were filled with clusters of parallel tubular cristae of varying complexity which at times enveloped islands of mitochondrial matrix and fingers of cytoplasm which projected into the mitochondrion. Aggregations of numerous mitochondria occupied much of the cytoplasm of highly altered cells. Modifications of this nature have not been described following ACTH stimulation of the adrenal cortex. This raises the distinct possibility that thyroid effects on the adrenal cortex are not entirely ACTH mediated.Since the observations of Hoskins ('10) it has been known that the administration of thyroid material to animals results in the hypertrophy of their adrenal glands. Adrenocortical hypertrophy after treatment with thyroxine or desiccated thyroid has been demonstrated in the rat (Cohen, '35 Although reports on the effects and the mechanism of thyroid-adrenal interaction have often conflicted, there can now be little doubt that thyroid hormone does have an influence on the adrenal cortex. The alterations in histology and function reported by numerous investigators should almost certainly be accompanied by changes in ultrastructure; however, no ultrastructural studies in support of such a conclusion have been recorded to this date. The purpose of this paper, therefore, is to describe the effects of hyperthyroidism on the fine structure of the rat adrenal cortex and possibly to shed additional light on the mechanism of thyroid-adrenal relationships. Although all zones of the adrenal cortex were examined, observations described in this report are limited to the zona fasciculata. MATERIALS AND METHODSAnimals used in this experiment were Tex/SDD adult male albino rats weighing 250-300 gm at the onset of the experiment. Alteration in available thyroid secretion was achieved by surgical thyroidectomy or radiothyroidectomy followed by treatment with desiccated thyroid and by thyroxine administration to intact animals. Short term hyperthyroidism was produced in two intact animals by the intraperitoneal injection of 250 pg of sodium levothyroxine per day for ten days. These animals were sacrificed 24 hours after the last injection. Long term hyperthyroidi...
Chronic hyperthyroidism was induced in radiothyroidectomized and surgically thyroidectomized adult male rats by feeding a diet of 0 3 4 . 4 % desiccated thyroid for four to ten week periods. Short term hyperthyroidism was induced in intact rats by the intraperitoneal injection of 250 pg/day of sodium levothyroxine for ten days. Adrenal glands were fixed by perfusion with 3% phosphate buffered glutaraldehyde and post-fixed in 1 % osmium tetroxide. The zona fasciculata of the adrenal glands from experimental and control animals was examined in the electron microscope. Drastic mitochondrial alterations characterized the zona fasciculata of hyperthyroid rats. Initially, mitochondria became more nearly round and contained increased numbers of paracrystalline tubular inclusions of the type described by Kjaerheim ('67) and Wheatley ('68).In more altered states many mitochondria were filled with clusters of parallel tubular cristae of varying complexity which at times enveloped islands of mitochondrial matrix and fingers of cytoplasm which projected into the mitochondrion. Aggregations of numerous mitochondria occupied much of the cytoplasm of highly altered cells. Modifications of this nature have not been described following ACTH stimulation of the adrenal cortex. This raises the distinct possibility that thyroid effects on the adrenal cortex are not entirely ACTH mediated.Since the observations of Hoskins ('10) it has been known that the administration of thyroid material to animals results in the hypertrophy of their adrenal glands. Adrenocortical hypertrophy after treatment with thyroxine or desiccated thyroid has been demonstrated in the rat (Cohen, '35 Although reports on the effects and the mechanism of thyroid-adrenal interaction have often conflicted, there can now be little doubt that thyroid hormone does have an influence on the adrenal cortex. The alterations in histology and function reported by numerous investigators should almost certainly be accompanied by changes in ultrastructure; however, no ultrastructural studies in support of such a conclusion have been recorded to this date. The purpose of this paper, therefore, is to describe the effects of hyperthyroidism on the fine structure of the rat adrenal cortex and possibly to shed additional light on the mechanism of thyroid-adrenal relationships. Although all zones of the adrenal cortex were examined, observations described in this report are limited to the zona fasciculata. MATERIALS AND METHODSAnimals used in this experiment were Tex/SDD adult male albino rats weighing 250-300 gm at the onset of the experiment. Alteration in available thyroid secretion was achieved by surgical thyroidectomy or radiothyroidectomy followed by treatment with desiccated thyroid and by thyroxine administration to intact animals. Short term hyperthyroidism was produced in two intact animals by the intraperitoneal injection of 250 pg of sodium levothyroxine per day for ten days. These animals were sacrificed 24 hours after the last injection. Long term hyperthyroidi...
In concert with studies of the effects of various pharmacologic inhibitors of corticosteroidogenesis on adrenocortical morphology, U-8113, an analog of amphenone B, was administered daily to Sprague-Dawley rats for 7, 14, 21 or 30 day. The primary morphological responses involved increases in adrenal weight, width of zona fasciculata, width of zona reticularis, intracellular lipids, mitochondrial size, mitochondrial vacuolation and crystalline-like inclusions, small coated vesicles, lysosomes, autophagic vacuoles and cholesterol ester clefts. In particular, the increases in lysosomes, coated vesicles and autophagic vacuoles containing morphologically altered mitochondria were considered reflective of mechanisms designed to maintain cellular integrity amidst functional impairment. Lipid analysis revealed marked increases in cholesterol esters and phospholipids, supportive of morphological observations. When permitted a 14 day recovery period following either 14 or 30 days of inhibitor therapy, most fine structural alterations and lipid derangements were diminished, and the cells approximated normal parameters.
The functional zonation in the adrenocortical tissue of the duck was experimentally investigated after chronic administration of corticosteroids of different types (corticosterone, desoxycorticosterone, dexamethasone) and salt loading (chlorides of sodium and potassium). The cytomorphology of the interrenal cells belonging to subcapsular and central zones was explored by light- and electron microscopy and by biochemical analysis of plasma corticosterone. Corticoid-induced involution of the interrenal tissue, or hyperactivity elicited by salt loading were evident in both subcapsular and central regions of the gland. In the duck the adrenocortical tissue appears to be devoid of steroidogenic functional differentiation. The modifications of different cellular organelles and inclusions can be explained in the light of known concepts about corticosteroid metabolism. The depression of plasma corticosterone titre in corticosteroid-treated animals agrees with the image of cytological inhibition. The lowered corticosterone value in KCl-loaded ducks signifies increased peripheral metabolism of this hormone. The hypercorticosteronemia in NaCl-loaded ducks is probably related to activation of the nasal gland under osmotic stress.
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