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Biomedical subjects

E A Baumanis

Publications and source records attributed to E A Baumanis.

17 recordsLinked to original sources
PubMed1989

[Cytological and immunological aspects of the antitumor action of polyhexamethylene guanidine in BALB/c mice].

Repeated intraperitoneal and intratumor administration of polyhexamethylene guanidine (PMG) in 3 and 5 mg/kg doses to sarcoma 180 bearing mice caused a significant reduction in tumour mass accompanied by increased incidence of diploid and hypodiploid cells. PMG brings about an increase in the number of activated macrophages in the spleen, whereas the response of antibody-producing cells (APC) varies with the dose. A single injection of PMG (1 mg/kg) caused stimulation, but under repeated administration and at higher doses the drug suppressed APC proliferation. The dose-dependent effects of PMG on humoral immunity was due to its specific influence on the spleen L-ornithine decarboxylase activity.

Animals↗
PubMed1981

Modification of the activity of mitochondrial monoamine oxidases in vitro and in vivo.

Treatment of bovine brain mitochondrial membranes with iproniazid (Ip) (1 mM, 15 min) inhibited monoamine oxidase (MAO) activity (substrates: 5-hydroxytryptamine, tyramine, dopamine) and significantly (about 7-fold) increased histamine deaminating activity (HDA). A selective inhibitor of MAO-A clorgyline (contrary to deprenyl) prevented the increase in HDA. Ip (200 mg/kg; within 10-16 h after parenteral administration) markedly (about 6-fold) increased the level of the HDA) in brain mitochondria of mice and guinea pigs. At the same time, a decrease in content of histamine (Hi) and increase in content of 5-hydroxytryptamine was noted in the brains of mice. In anesthetized and non-anesthetized guinea pigs Ip decreased (or prevented) the bronchoconstriction and toxic effects caused by Hi. The antihistamine effects of Ip are apparently due to its being able to induce reversible qualitative alteration (transformation) of the catalytic activity of the membrane-bound MAO of type A, which acquires as a result of this transformation potent HDA.

Animals↗
PubMed1978

[Development of experimental brain tumors in modulated amine metabolism].

There was found a correlation between dynamic changes in the serotonin level and mortality in rats with 9,10-dimethyl-1,2-benzanthracene induced blastomogenesis. An estimation was made of the influence of monoamine oxidase inhibitors, transamine and D, L-malic acid benzyldihydrazide on the type of a tumor produced. Chemical blastomogenesis in the case of cerebellar tumors is shown to be associated with the decreased serotonin content at the site of a tumor. But fluctuations of the serotonin level in the hypothalamus have not been detected. This evidenced that the decreased mortality rate caused by the administration of monoamine oxidase inhibitor is due to a lower production of astrocytomas and genetically related glioblastomas. The role of serotonin in increasing the astrocyte resistance to malignant degeneration has been discussed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

[Multiplicity of monoamine oxidase: inhibition of mitochondrial monoamine oxidase activity by isopropylhydrazide of D,L-serine].

Isopropylhydrazide of D,L-serine (IHS) inhibits by 50% (at 37 degrees for 10 min) deamination of serotonin or beta-phenylethylamine by monoamine oxidases from bovine brain stem mitochondrial membranes at the 2.6 X X 10(-5) M or 9 X 10(-5) M, respectively. In order to inhibit by 50% the deamination of tyramine under the same conditions a considerably lower (2.5 X X 10(-6) M) concentration of IHS is required. Kinetic studies of inhibition of enzymatic deamination of all the three biogenic monoamines by IHS showed that the irreversible blocking of the monoamine oxidase activity is preceeded by formation of dissociating enzyme-inhibitor complexes. Values of the dissociation constants of these complexes measured (at 37 degrees) with serotonin, phenylethylamine or tyramine as substrates for estimation of the residual monoamine oxidase activity are 0.47; 0.13 or 0.023 mM, respectively. Significant differences are also found between thermodynamic and activation parameters characterizing both both steps of interaction between IHS and the monoamine oxidases of mitochondrial membranes in the experiments with serotonin, phenylethylamine or tyramine as substrates. The data obtained suggest the existence of different monoamine oxidases (or their active sites) catalyzing oxidative deamination of serotonin, phenylethylamine or tyramine in the fragments of mitochondrial membranes from bovine brain stem.

Animals↗
PubMed1976

[Comparative study of the effect of inhibitors of monoamine oxidase and ftorafur on the growth of de-differentiated astrocytoma].

To evaluate the possible antitumour effect of intensified deposition of serotonin in the region of localization of the tumour caused by a pharmacological preparation studies of the effect of inhibitors of monoamine oxidase transamine and N2N2-dibenzylhydrazide of DL-malic acid on rat's cerebellum tumour de-differentiated by astrocytoma (strain No 101/12) were carried out. The effect of inhibitors of monoamine oxidase was compared with that of antiblastic preparation of phthorafur. Differences in the mechanisms of action of pharmacological agents referred to above are shown. It was established that inhibitors of monoamine oxidase administered against the background of the developing tumour caused a considerable reduction in its weight and prononced dystrophic and necrotic changes.

Animals↗
PubMedDate not supplied

[The modification of the catalytic activity of mitochondrial monoaminoxidase and the suppression of the growth of experimental brain tumors].

A derivative of pyrazinocarbazole the antidepressant pyrazidol, whose inhibition of serotonin deaminase activity of the brain mitochondrial monoamine oxidase is attended by induction of the property of catalysing histamine oxidation, inhibits the growth of glial tumors in experiments. Another derivative of pyrazinocarbazole, which inhibits serotonin deamination but does not induce the appearance of histamine deaminase activity, produces no effect on the growth of glial tumors of the brain.

Animals↗
PubMedDate not supplied

[Effect of aminoxidase activity regulators on the humoral immune response and proliferation of lymphoid and nonlymphoid cells].

DL-malic acid dibenzylhydrazide (I) and dihydrazide (II), inhibitors of aminoxidases, have been shown to inhibit immune reactions when administered at the phase of initiation but to stimulate the immune response and proliferation of lymphoid and nonlymphoid cells if given on the 2nd and 3rd day following immunization when the immune reaction is in progress. The intensity of local allergic reaction during passive skin anaphylaxis is reduced by I and enhanced by II if the compounds are administered 16 hrs prior to antigen challenge.

Anaphylaxis↗
PubMedDate not supplied

[Mechanism of the qualitative modification of mitochondrial monoamine oxidase activity by pyrazidol].

Inhibitory effect of pyrazidol (I) on serotonin-deaminating activity in mice brain mitochondria, which was accompanied by induction in this source of monoamine oxidase (MAO) of a property to oxidize histamine, was distinct from the effect of 3,3a-dehydroderivative of pyrazidol (II), which did not induced the histamine deaminating activity. Analysis of electron absorption spectra and polarographic studies demonstrated that inhibition of MAO by pyrazidol resulted in dehydration of the piperazine ring in the molecule of the drug as well as in possible formation of azomethine bond at the 2-3 position, exhibiting high oxidizing activity. At the same time, marked alterations in the substance II structure were not found in the course of inhibition of serotonin-deaminating activity in mitochondria. As pyrazidol did not exhibit pro-oxidant activity, its azomethine group appears to have a direct oxidating activity, which was not mediated via lipid peroxides.

Animals↗
PubMedDate not supplied

[Effect of D,L-malic acid dibenzylhydrazide on changes in the antioxidizing activity of lipids and monoamine oxidase activity in mouse organs].

Administration of dibenzylhydracide of D,L-malic acid (inhibitor of monoamine oxidase) into animals caused not only inhibition but also transformation of the mitochondrial monoamine oxidase activity, which acquired the property to deaminate histamine. Effect of the monoamine oxidase inhibitor on the antioxidative activity of lipids from mouse liver and brain tissues was studied. Effect of the dose administered and of the period of its action after administration were characterized. Influence of the inhibitor on oxidation of methyloleate was also studied in a model system. The data obtained suggest that the transformation-producing effect of the substance was not related to its immudiate action on the enzyme molecule but was apparently due to its influence on the intensity of lipid peroxidation in membranes.

Animals↗
PubMedDate not supplied

[Effect of the antihistamine preparation, fencarol, and other quinuclidyldiarylcarbinols on tissue aminoxidase activity].

In experiments in vivo, the derivatives of quinuclidylarylcarbinol, possessing an antihistaminic activity, fencarol, its di(o-tolyl)- and di(o-methoxyphenyl)-derivatives activate histamine oxidative deamination by diaminoxidase of the rat lungs and increase the histamine tissue level. Quinuclidyl-3-dithienyl carbinol inhibits the activity of diaminoxidase, but decreases the histamine tissue level. On the contrary, dimedrol (diphenhydramine), pipolfen (promethazin), pyrilamine and cyproheptadin exerted no effect on the activity of diaminoxidase or the histamine tissue level. All the compounds studied did not alter oxidative deamination of the rat brain serotonin by monoamine oxidase or the serotonin content in brain tissues.

Animals↗
PubMedDate not supplied

[Modification of mitochondrial monoamine oxidase activity by certain amine inhibitors].

Monoamine oxidase inhibitors /trans-2-phenylcyclopropylamine, pyrazidol, phenharmane/ belonging to the category of primary or secondary amines, in the molecule of which/ after dehydration/ formation of an azomethine bond is possible, modified the activity of membrane bound bovine brain monoamine oxidases inhibiting the deamination of serotonin and, at the same time, causing appearance of or significant increase in cadaverine--or histamine--deaminating properties. This modification was not caused either by primary amines /amphetamine, GABA/ which are not potent monoamine oxidase inhibitors or by the amines possessing strong monoamine oxidase inhibiting properties/pargylline, deprenyl, harmine/ but devoid of the potential property of forming an azomethine bond. In vivo trans-2-phenylcyclopropylamine, pyrazidol or phenharmane /contrary to amphetamine/ did modify the monoamine oxidase activity in brain of mice inducing the deamination of histamine and decreasing its tissue concentration.

Amphetamine↗
PubMedDate not supplied

[Effect of serotonin and monoamine oxidase inhibitors on corneal anesthesia produced by celnovocaine and novocaine].

In experiments on guinea pigs it is shown that a preliminary intraperitoneal administration of monoamine oxidase inhibitors (MAOI) -- transamine (10 mg/kg) or malic acid benzyldihydrazide (50 mg/kg) antagonizes the local anesthetic action of celnovocaine (CC) and novocaine (NC). An analogous effect is also observed following instillation of transamine (a 0.1% solution) and malic acid benzyldihydrazide (a 0.23% solution) into the eye 10 minutes before administration of the anesthetic. Instillation of a 0.1% serotonin creatinine sulphate solution also antagonizes anesthesia produced by CC and NC, while MAOI potentiates the effect of serotonin.

Anesthesia, Local↗