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At least 91 records · Page 5Linked to original sources
PubMed1978

Nuclear-magnetic-resonance study of aggregations and conformations of melanostatin and related peptides.

The 1H and 13C nuclear magnetic resonance spectra of melanostatin (Pro-Leu-Gly-NH2) and related peptides (Pro-Leu-Gly, Z-Pro-Leu-Gly, Z-Pro-Leu-Gly-NH2 and Z-Pro-Leu-Gly-OCH3, where Z = benzyloxycarbonyl) were analysed in a variety of solvents. At physiological pH, the melanostatin molecule is N-protonated in aqueous solution. The concentration dependences of the chemical shifts of amide-proton and carbonyl-carbon resonances and of proton spin-lattice relaxation times were observed in relation to molecular aggregations. In dimethylsulfoxide solution, aggregations were observed for N-protonated melanostatin and Pro-Leu-Gly prepared with HCl and for the Na salt of Z-Pro-Leu-Gly but not for N-protonated melanostatin prepared with HClO4 or HNO3, unprotonated melanostatin, Z-Pro-Leu-Gly-NH2, or Z-Pro-Leu-Gly-OCH3. The leucine NH and glycine CO groups of N-protonated melanostatin are involved in the intermolecular hydrogen bonds of aggregates. The leucine NH group of N-protonated Pro-Leu-Gly also forms the intermolecular hydrogen bond. The solvent and temperature dependences of the chemical shifts of amide-proton and carbonyl-carbon resonances were measured to determine intramolecular hydrogen bonding. In dimethylsulfoxide solution, N-protonated melanostatin molecules in part take the beta-turn structure and the trans carboxamide NH proton and carbonyl oxygen of the proline residue form an intramolecular hydrogen bond.

Glycine↗
PubMed1977

Effect of estrogen and progesterone on the release of MSH in gonadectomized rats.

The concentration of MSH in serum after estrogen or progesterone injection into gonadectomized rats was measured by a biological assay. Undetectable serum MSH values were found in long-term ovariectomized (OVX) rats. After a single injection of 10 microgram estradiol benzoate (EB) serum MSH exhibited a circadiam rhythm with high levels in the afternoon, while values in the morning were negative. This effect occurred for 4 days following the injection. Progesterone injection into spayed rats also resulted in an increase of serum MSH concentration, but in contrast to the changes observed after EB treatment high values were found in the morning for 3 consecutive days. Afternoon MSH levels were low but measurable. The effect of these steroids on the activity of the hypothalamic enzymes which yielded MIF or MRF upon incubation with oxytocin (OXT) was also studied. Enzymatic activity of both systems was undetectable in OVX rats and was evident after EB treatment. Progesterone increased only the activity of the system which yields MRF. In castrated male rats estrogen elevated baseline MSH levels but a circadian rhythm was not observed, whereas progesterone had no effect. These observations demonstrate a sex difference on steroid-induced MSH release.

Animals↗
PubMed1978

Dose-related biphasic effect of prolyl-leucyl-glycinamide (MIF-I) in depression.

Five of 8 patients with unipolar or bipolar endogenous depressions taking prolyl-leucyl-glycinamide (MIF-I), 75 mg/day, showed substantial improvement within a few days of beginning treatment compared with similar improvement in only 1 of 10 receiving 750 mg/day of MIF-I and only 1 of 5 patients taking placebo. The lower dose of MIF-I was associated with significantly greater improvement than both the higher dose and placebo on all of the rating scales used. The authors suggest that an even lower dose of MIF-I, on the order of 0.1 mg/kg, may have a greater effect as an antidepressant.

Adult↗
PubMed1977

Synthetic MIF analogues. Part II: Dopa potentiation and fluphenazine antagonism.

A comparison is described between the activity of the melanocyte-stimulating hormone release inhibiting factor (MIF) and those of five synthetic tripeptide analogues of MIF. The comparison was based upon the ability of the compounds to potentiate the behavioral effects of L-dopa in mide and to antagonize fluphenazine-induced catalepsy in rats. Three of the tripeptides potentiated L-dopa in a manner similar to that of MIF. All of the synthetic analogues antagonized fluphenazine after a single dose although their potency and their duration of action differed. MIF was active in the latter test only following chronic administration. The possible mechanism of action and the potential clinical applicability of the tripeptides are briefly discussed.

Animals↗
PubMed1978

[Physiological trials with MIF-I in Parkinson's disease (author's transl)].

The writers present some physiological (and not therapeutic) acute and sub-acute trials with tripeptide: L-propyl-L-leucyl-glycine amide (M.I.F.-I) in Parkinson's Disease. This work confirms the earlier observation that M.I.F.-I employed alone or in combination with Levodopa is active against Parkinson's disease. The writers evoke the hypothesis that this action takes place at the postsynaptic receptors, whose configuration may be modified in the sense of a hypersensitivity. These studies justify undertaking a series of controlled therapeutic trials when the cost of the product permits and as well instituting development work on analogues active orally.

Aged↗
PubMed1977

New evidence that demonstrates that L-pro-L-leu-L-gly-NH2 might be the natural MIF.

A wide range of doses was used to study the effect of Pro-Leu-Gly-NH2 (MIF) on the MSH release in rat pituitaries incubated in vitro. The Pro-Leu-Gly-NH2 was added to one half of the gland, and the other was used as control. The MSH released into the medium was measured by a bioassay and the activity of the samples referred to a standard of synthetic alpha-MSH. Pro-Leu-Gly-NH2 in doses of 10 to 30 ng/ml inhibited the MSH release in about 60%. Doses between 10(3) to 10(4) ng/ml induced neither release nor inhibition of the release of MSH. Dose of 10(5) ng/ml clearly induced release of MSH. The results of the additional experiments presented, although they represent no proof, are in line with the contention that Pro-Ley-Gly-NH2 in the natural MIF.

Animals↗
PubMed1976

Double-blind evaluation of oral L-prolyl-Lleucyl-glycine amide in Parkinson's disease.

A 4-month double-blind study comparing the effect of increasing oral doses (up to 1.0 g daily) of synthetic L-proyl-L-leucyl-glycine amide (PLG) and placebo in 20 parkinsonian patients showed no significant improvement in objective scores of functional disability. However, important trends and some significant results were observed with the lower doses of PLG. These essentially negative results may be attributed to poor intestinal absorption of the compound, a short biologic half-life in the blood, or administration of oral doses that were much higher than required, or a combination of factors. In further studies with this peptide, which are encouraged, the intravenous route should be used until the question of intestinal absorption is resolved.

Adult↗
PubMed1978

[The influence of MIF (melanocyte-stimulating hormone-release inhibiting factor) on psychomotor function and mood in parkinsonian patients. Preliminary report (author's transl)].

In 12 parkinsonian patients aged from 40--76 years the L-dopa-potentiating effect of MIF was investigated using a doubleblind crossover design. MIF was given i.v. in a dose of 200 mg. The following psychological tests were carried out 4 times after the injection of MIF at hourly intervals: Purdue pegboard, Minnesota-Rate of manipulation test, 2-key-tapping, simple and complex reaction time and a state of well-being scale. The results revealed a marked effect on finger dexterity, drive and complex reaction time. That means MIF does not only lead to an improvement of psychomotor performance but also of cognitive functions. In contrast thereto the influence on the state of well-being was less impressive.

Adult↗
PubMed1975

[Infusion therapy with mif (melanocyte inhibiting factor) in Parkinson's disease (author's transl)].

On the basis of reports in the literature and of our own clinical experience it appears that melanocyte inhibiting factor (MIF) is a very promising therapeutic agent in the management of Parkinson's disease. Besides theoretical considerations relating to biochemical and pathophysiological spheres, the question of the current dosage for clinical usage seems to be of the utmost importance. We are of the opinion that the currently-employed dosage of 400 mg daily is still too low. Hence, the present investigation will be continued with a view to establishing the optimum dosage for maximal therapeutic effect.

Aged↗