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Biomedical subjects

H Seim

Publications and source records attributed to H Seim.

35 records · Page 2Linked to original sources
PubMed1985

[Stimulation of leukocyte migration by L-carnitine].

In order to stimulate the vitality and growth of cell cultures, serum from calves or horses is frequently added to different concentrations. It is only in serum-free systems, however, that exactly defined constant conditions of cultures can be created and that cellular regulating factors can be characterized in a biochemical way. From this aspect we investigated the impact of L-carnitine on leukocyte migration in vitro. In a serum-free medium a significant stimulation of migration could be identified in 6.2 mmol/l of L-carnitine by means of the agarose-microdroplet technique. Even those concentrations of carnitine which elicited no significant stimulation resulted in a homogeneous distribution of cells on the migrating area, thus unequivocally limiting the distance of migration. An unspecific effect of concentration or ions was excluded by the application of gamma-butyrobetaine which did not produce any stimulation of migration. Even lymphokine activity (leukocyte inhibitory factor of migration) could be represented after having added carnitine.

Betaine↗
PubMed1985

The response of some intravascular and intracellular lipid parameters of the rat after treatment with isatin.

The effect of isatin on serum lipid concentrations, the activity of lipoprotein lipase, the activity of lipogenic enzymes and the oxidation rate of fatty acids of female Wistar rats were investigated. A decrease of the triglyceride concentrations could be observed after one week of treatment of the group of sucrose-rich alimented animals, after two weeks this was also the case with the group fed with standard food. There were no changes in the cholesterol concentrations. Post-heparin lipolytic activity was not influenced. The liver enzymes malic enzyme, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase showed a remarkable increase in activity. The simultaneous rise of the oxidation rate of 14C-palmitate in the liver was measured. On the basis of the present findings the accelerated degradation rate could be responsible for the hypolipemic effect of the substance. The possible participation of the carnitine shuttle in the lipid-lowering action is discussed on the basis of changed concentrations of total carnitine, free carnitine and acylcarnitine in pooled serum samples after treatment with isatin.

Animals↗
PubMed1983

A new dysfibrinogenemia: fibrinogen Oslo IV.

A family with dysfibrinogenemia is described. The abnormal fibrinogen occurred in three successive generations indicating a dominant hereditary pattern. Thrombin and reptilase times were about twice the normal value. This was shown to be caused by a polymerization defect, fibrinopeptide release being normal. Platelet aggregation was undisturbed, indicating normal platelet-fibrinogen binding. The bleeding time was normal and there was no bleeding tendency. However, an obscure recurrent pulmonary ailment may, or may not, be related to the dysfibrinogenemia. The abnormal fibrinogen was tentatively termed Oslo IV.

Amino Acid Sequence↗
PubMed1983

[Chronotropic effects of carnitine derivatives in isolated rabbit atria at defined transmural pressures].

Acetylcarnitine isomers and gamma-betaine methylesters are closely structure-related to cholinergic agonists. With continuous perfusion at defined transmural pressures of 0.1 and 0.5 kPa their effects on the chronotropic autoregulation of isolated spontaneously beating atria were examined in comparison with acetylcholine. Independent of the transmural pressure, the two isomers of acetylcarnitine had no effects on the heart rate up to a concentration of 10(-3) mol/l. Among the carboxylesters of gamma-betaines, the crotonobetaine methylester was up to 100 fold more effective than acetylcholine. Hydrogenation of the double bond decreased the negative chronotropic response 10 times. The L(-)-carnitine-methylester did not influence the spontaneous heart rate up to 3 X 10(-3) mol/l, but the D-isomer inhibited it significantly. Increase of the transmural pressure caused the same level of heart rate in both controls and atria under free betaines. At transmural pressure of 0.5 kPa, in comparison with 0.1 kPa, a significantly greater impairment of heart rate, released by crotonobetaine-methylester, was observed. Atropine blocked the interactions of the gamma-betaine-methylesters with the muscarinic cholinergic receptors of the pacemaker cells.

Animals↗
PubMed1982

Stimulation of the anaerobic growth of Salmonella typhimurium by reduction of L-carnitine, carnitine derivatives and structure-related trimethylammonium compounds.

In view of the development of a L-carnitine deficiency, the metabolism of L-carnitine and structure-related trimethylammonium compounds was studied in Salmonella typhimurium LT2 by means of thin-layer chromatography (TLC). L-Carnitine, crotonobetaine and acetyl-L-carnitine stimulated the anaerobic growth in a complex medium significantly. The stimulation depended on the formation of gamma-butyrobetaine. The reduction of L-carnitine proceeded in two steps: (1) Dehydration of the L-carnitine to crotonobetaine, (2) hydrogenation of crotonobetaine to gamma-butyrobetaine. The reduction of crotonobetaine was responsible for the growth stimulation. Terminal electron acceptors of the anaerobic respiration such as nitrate and trimethylamine N-oxide, but not fumarate, suppressed the catabolism of L-carnitine completely. Glucose fermentation, too, inhibited the reduction of L-carnitine but optimal growth with a high carnitine catabolism was achieved by D-ribose. The esters of carnitine with medium- and long-chain fatty acids inhibited the growth considerably because of their detergent properties.

Anaerobiosis↗
PubMed1980

[Catabolism of carnitine: products of carnitine decarboxylase and carnitine dehydrogenase in vivo].

1) Rats and mice were given large oral or subcutaneous doses of (-)-L-, (+)-D- and DL-carnitine (5 mg/g body weight). The carnitine metabolites, beta-methylcholine and acetonyltrimethylammonium, were isolated from the urine by special methods, and determined as their characteristic derivatives (2,4-dinitrophenylhydrazone and butyric ester) by thin-layer chromatography or photometry. 2) beta-Methylcholine, the product of carnitine decarboxylase, was not excreted, even when animals were heavily dosed with both carnitine isomers, with or without starvation. 3) After the administration of (+)-D- and DL-carnitine, both species excreted acetonyltrimethylammonium, which is already known as the spontaneous decarboxylation product of dehydrocarnitine (product of carnitine dehydrogenase) in bacteria. Injection of 0.71 mmol (+)-D-carnitine resulted in the excretion of 5.0 mumol (average) acetonyltrimethylammonium per mouse during the 48 h post injection. Under the same conditions, rats produced up to 40 mumol acetonyltrimethylammonium. The ratio of excreted acetonyltrimethylammonium to injected (+)-D-carnitine depended on the method of administration and the dose. 4) Production of the pharmacologically active (+)-acetyl-L-beta-methylcholine is not to be expected, following high exogenous doses of (-)-L-carnitine or (-)-acetyl-L-carnitine. The chief metabolites are trimethylamine, trimethylamine oxide and gamma-butyrobetaine (this journal 361, 1059), and both the (-)-L-carnitine pool and exogenous (-)-L-carnitine are dehydrogenated or decarboxylated only to a very small extent, if at all. When DL-carnitine is used therapeutically, the formation of acetonyltrimethylammonium must be taken into account.

Administration, Oral↗
PubMed1978

[Interrelationships between carnitine metabolism and fatty acid assimilation in Pseudomonas putida (author's transl)].

The carnitine metabolism and some relations to the fatty acid metabolism were studied in Pseudomonas putida by means of control of growth, analysis of metabolites, and determination of enzyme activites. The strain grew on gamma-butyrobetaine, D,L- and L-carnitine, glycinebetaine, choline, D,L-norcarnitine, D,L-gamma-amino-beta-hydroxybutyrate, and D,L-beta-hydroxybuty-rate. Although the strain used straight-chain fatty acids of 2-16 C-atoms, it was only able to grow on O-acyl-L-carnitines of 10 or more C-atoms in the acyl-group. Addition of carnitine stimulated the growth on long-chain fatty acis. The formation of trimethylamine increased, if L-carnitine or gamma-butyrobetaine were the only carbon sources, and decreased, if these trimethylammonium compounds were carbon as well as nitrgen sources. L-Carnitine induced the carnitine dehydrogenase as well as the beta-hydroxybutyrate dehydrogenase, gamma-Butyrobetaine as carbon and nitrogen source induced the carnitine dehydrogenase, too. In the crude extract the specific activiteis of beta-hydroxybutyrate dehydrogenase were 0.7 or 1.6 mumoles.min-1.mg-1 after growth on L-carnitine and D,L-beta-hydroxybutyrate, respectively. The synthesis of both enzymes was repressed by glycinebetaine, glucose and long-chain fatty acis. Dependent on the nitrogen source L-carnitine was catabolized via two different pathways.

Animals↗
PubMed1978

[Induction of mitochondrial volume changes by homologous O-acyl carnitines].

The volume changes of isolated rat liver mitochondria induced by O-acylcarnitines are dependent on the optical isomery and the length of the apolar hydrogen chain in the acyl residue. Within the homologous series of the straight-chain O-acyl carnitines the swelling-inducing effect increases from decanoyl carnitine to the palmitoyl carnitine. The contraction is observed only under the effect of O-acylL(--)carnitines, while isomers add up in their swelling-inducing effect. The surface activity of the O-acyl carnitines increases with increasing chain length, and the critical micellar concentration decreases logarithmically. The comparison of the tenside properties with the swelling- and contraction-inducing effects shows that the swelling is brought about by hydrophobic interactions with the membranes, while the contraction is the consequence of energy-dependent metabolic processes which are connected with the influx of acyl carnitines and the efflux of the ions from the mitochondria.

Animals↗
PubMed1977

[Utilization of trimethylammonium-compounds by Acinetobacter calcoaceticus (author's transl)].

The utilization of carnitine and carnitine derivatives (O-acylcarnitines, carnitine carboxylderivatives) and structure-related trimethylammonium-compounds (betaines and nitrogen-bases) by Acinetobacter calcoaceticus was studied by means of the control of growth and the quantitative detection of metabolites. The strain grew only on L-carnitine, L-O-acylcarnitines, and gamma-butyrobetaine as the sole carbon sources. The utilization of these compounds and the growth correlated with the cleavage of the C-N bond and thereby with the formation of trimethylamin. D-Carnitine was metabolized, if an additional carbon source, like L-carnitine, was present in the incubation mixture, or if the bacteria were preincubated with L- or DL-carnitine, but no growth was observed on D-carnitine as the sole carbon source. The bacteria oxidized choline to glycinebetaine in the presence of additional carbon sources, glycinebetaine itself was not assimilated. With regard to the catabolism of quaternary nitrogen compounds Acinetobacter calcoaceticus shows a different pathway in comparison with other bacterial species metabolizing carnitine.

Acinetobacter↗
PubMed1976

[L-carnitine as a basis of cholinomimetic substances].

Acetylcarnitine, though having the same configuration as acetylcholine and Acetyl-beta-methylcholine, is devoid of cholinomimetic properties as long as the carboxylic group is free. Contrary findings are explainable by the lack of uniformity of the test substance, caused by substitution of the carboxylic group and intramolecular cleavage of water or acetic acid from carnitine or acetylcarnitine and by admixtures of active substances, and are attributable to the formation of metabolites in vivo. Already the recrystallization of salts of L-acetylcarnitine and L-carnitine in alcohols causes the formation of active carboxylic esters. The latter can be separated and identified by t.l.c. from the starting substances. At the isolated frog heart (Rana esculenta), neither L-carnitine nor L-acetylcarnitine have muscarine-like effects; higher concentrations of them (0.03-0.15 M) exert positively inotropic effects that increase with concentration and are qualitatively and quantitatively equal for L-carnitine and lower O-acyl-L-carnitines. As betaine, L-carnitine affects the heart rate only at 42 +/- 12 mg/ml, crotonic acid betaine at 22 +/- 7 mg/ml, gamma-butyrobetaine at 15 +/- 8 mg/ml. As a result of carboxyl substitution of betaines, the cholinomimetic properties increase to the level of the stimulation system choline/acetylcholine. The LD50 of L-acetylcarnitine for mice injected s.c. with 8.4 (7.3-9.7) mg/g body weight is within the range of LD50 of L-carnitine. Both substances, even when administered in high doses, give no such symptoms as cholinomimetic substances. Carnitine carboxyl ester, acetylcarnitine carboxyl ester, and other carnitine derivatives, on a molar basis, are 2-10(1) to 2-10(3)-fold more toxic than carnitine and acetylcarnitine. The modes of action of carnitines and their metabolites upon the heart rate are discussed.

Animals↗