Effects of glucocorticoid treatment of the carbonic anhydrase activity of brain tissue in the early postnatal age in the rat.

The carbonic anhydrase activity in the brain tissue shows a considerable increase with proceeding gliogenesis during the first three postnatal weeks in the rat. The administration of 10 to 30 micrograms corticosterone or 5 to 10 micrograms dexamethasone per g body weight to 3-day old rats produced a marked acceleration in maturation of enzyme activity in the neocortex and hippocampus. The noradrenaline-induced stimulation of enzyme activity under in vitro conditions was also enhanced in corticosterone pretreated rats. There was no difference between the influence of noradrenaline and cAMP on stimulation of enzyme activity in either control or glucocorticoid-pretreated rats. In contrast to the corticosterone, the pretreatment with dexamethasone failed to stimulate the noradrenaline or cAMP effects on enzyme activity which may be due to differences in receptor-mediated responses for glucocorticoids. The glucocorticoid-induced acceleration of enzyme activity in the early postnatal period may be attributed to an enhanced development of glial elements.

Effects of ACTH 1-24 on hydrolysis of beta-casomorphin-4-nitroanilide in brain homogenates in vivo and in vitro.

Administration of ACTH 1-24 to 3-10 days old rats produced a significant decrease in hydrolysis of beta-casomorphin-4-nitroanilide (beta-CM-4NA) in the cytosolic fraction of brain homogenate in the first three hours after injection. Corticosterone treatment did not modify the hydrolysis of the substrate. ACTH 1-24 but not ACTH 4-10, Met-enkephalin or Leuenkephalin given to the brain homogenate resulted in a dose-dependent decrease in liberation of 4NA from beta-CM-4NA. Kinetic data suggest competitive inhibition of ACTH molecule on hydrolysis of beta-CMA-4NA. The ACTH treatment, however, did not influence the hydrolysis of Pro-Gly-4NA or Pro-Pro-4NA in the brain homogenate in vitro.

Effects of systemic and intracerebral administration of glucose oxidase on the blood sugar level in rats.

Intravenous administration of 10 to 40 U/g b.w. glucose oxidase produced hypoglycaemia in a dose-dependent manner. The enzyme-induced drop of the blood sugar level was associated with significant rise in serum potassium and the concentration of free fatty acids. Intracerebral application of glucose oxidase through chronically implanted cannula into the ventromedial, lateral hypothalamus, preoptic region and amygdaloid complex of nuclei failed to change the blood sugar level, although a moderate increase of the free fatty acids and corticosterone concentrations occurred. The local application of enzyme in the locus coeruleus region led to a significant rise of the blood sugar concentration. The observations suggest the sensitivity of brainstem catecholaminergic neuronal system to hypoglycaemia.

Dipeptidyl peptidase IV (DP IV) and superoxide dismutase activity in thymus-derived lymphocytes: effects of inhibitory peptides and Zn2+ in vitro.

DP IV and superoxide dismutase (SOD) activity in thymus-derived lymphocytes of rats was assayed in vitro. The DP IV activity was measured fluorimetrically by hydrolysis of Leu-Pro-AMC, and the SOD activity by the inhibition of autooxidation of L-adrenaline. In order of their competitive inhibitory potency the following peptides were tested against DP IV and SOD activity: Ile-Pro-Ile (diprotin A), Val-Pro-Leu (diprotin B), Ile-Pro, Leu-Pro, Val-Pro, Tyr-D--Ala-Ala-Pro, Phe-Pro, Tyr-Pro, Ala-Ala-Pro and Gly-Pro. The peptides, in the order of their potency against DP IV, were effective to inhibit the SOD activity in T lymphocytes. Zn2+ ions exerted an inhibition on both DP IV and SOD activity in a near equimolar concentration. The involvement of Zn2+ as well as the peptides liberated by hydrolysis of polypeptides in regulation of cell-mediated immune responses has been discussed.

Superoxide dismutase activity in thymus cell suspension: effects of methionine-enkephalin and morphine.

Superoxide dismutase activity of rat thymus-derived cells was studied by the inhibition of L-adrenaline auto-oxidation oxidation in vitro. The incubation of cells in the presence of methionine-enkephalin (Met-Enk) or morphine (2-20.10(-7) M and 2-8.10(-6) M, respectively) was performed in Krebs-bicarbonate buffer at 37 degrees C for 180 min. After a lag period of 30 to 60 min of incubation, both Met-Enk and morphine decreased the inhibitory activity of cell suspension on the adrenaline autooxidation. Naloxone blocked the effects of opioids in near equimolar concentrations. The observations suggest the interaction of opioids on superoxide anion production of T cell lymphocytes.

Somatostatin-induced inhibition of lipolysis: in vitro studies.

Incubation of epididymal fat tissue slices with somatostatin (SS) led to the inhibition of epinephrine-induced release of free fatty acids (FFA) and glycerol in a dose-dependent manner. The SS administration did not suppress the lipolysis evoked by dibutyryl cAMP. The experimental findings indicate that SS exerts an inhibition of catecholamines-induced lipolysis at the level of adipocytes although the mechanism of action requires further investigations.