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Effects of angiotensins II (AngII), angiotensin IV (AngIV, 3-8 fragment of angiotensin II) and losartan (an antagonist of angiotensin receptor type 1) on the proliferation of adrenocortical cells in ovariectomized rats have been studied. The incorporation of bromodeoxyuridine (BrdU) into cell nuclei was used as an index of cell proliferation. AngIV decreased BrdU labeling index mainly in the reticularis zone and losartan (Los) was able to partially reverse this inhibitory effect of AngIV. AngII had no effect on the adrenocortical cell proliferation when given alone, however Los given simultaneously diminished BrdU incorporation into nuclei of glomerulosa and reticularis zones as compared with AngII. These findings suggest that AngII and AngIV modulate adrenocortical cell proliferation in ovariectomized rats.
The aim of the study was to determine the relation between involution of the FZ and the proliferation and apoptosis of the adrenal cortex cells. The study was carried out with adrenal glands from guinea pigs aged 1, 3, 9, 14, 21, 35 and 90 days. Paraffin slices were stained with Mayer haematoxylin and eosin and with acid fuchsin. For the immunohistochemical reaction the Anti- -PCNA Clone PC10 (Dako) was used. Apoptosis evaluation was performed with use of the TUNEL method (Roche). The results support the theory of involution of the FZ cells realised mainly by way of apoptosis. Analysis of the distribution and number of PCNA-positive cells in the adrenal cortex on subsequent days of PD may also back up the migration theory of renewal of the adrenal cortex cells.
The aim of the study was the evaluation of changes in the adrenal cortex lysosomal enzymes activity during experimental alloxan-induced diabetes mellitus in rabbits. We checked the activity of acid phosphatase, β-D-galactosidase, N-acetyl-β-D-glucosaminidase (NAGL) and lipase. The study was performed on 124 rabbits divided into five groups: one control and four experimental. Diabetes mellitus was induced by a single injection of 10% alloxan solution into the auricular vein in a dose of 10 mg per kg body weight. Animals from experimental groups were killed in the 21st, 42nd, 90th and 180th days of the study. Adrenal glands were removed. Enzymes activity was assayed by spectrophotometric methods. Changes in free and bound fractions of examined lysosomal enzymes activity were noticed already in the 21st day of diabetes. The most escalated changes were observed in the 42nd day of the study. Performed statistical variance analysis demonstrated statistically highly significant differences for activity of both fractions of NAGL and lipase, as well as for free fraction activity of acid phosphatase and β-D-galactosidase. The obtained data confirmed the influence of diabetes mellitus on changes in the activity of examined lysosomal enzymes in the adrenal cortex.
The impairment of homeostatic mechanisms in ageing becomes often apparent upon physiological or pathological stimulation. We have previously shown that fasting and refeeding revealed the existence of age-related changes of carbohydrate and lipid metabolism. Because fuel metabolism is partially controlled by corticosteroids we decided to determine the effects of refeeding on adrenal gland morphometry, ACTH, and corticosterone serum levels in young (5 mo) and (20 mo) old male Wistar rats. Fasting for 48 h did not change serum ACTH and corticosterone in both age groups. ACTH level did not change after 24 h of refeeding in young and old rats. However, in old, but not young animals, refeeding resulted in the decrease of corticosterone serum concentration. The relative weight of adrenal gland (% of body weight) did not change significantly with age (p=0.05). Fasting for 48 h induced in old rats but not in young ones increase of relative adrenal weight, and the volume of the reticular zone. Refeeding reduced adrenal volume, fascicular zone and reticular zone. Refeeding for 24 h decreased the total volume of adrenal gland of old rats due to a decline of the volumes of fascicular and reticular zones. In young rats refeeding reduced the volume of reticular zone. It is concluded that refeeding revealed ageing-dependent decline in the secretion of corticosterone, the key hormone of prolonged stress response.
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