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[The use of pantothenic acid preparations in treating patients with viral hepatitis A].

Calcium pantothemate in the daily dose 300 mg and 600 mg and pantetheine in the dose 90 mg and 180 mg per os were applied for 3-4 weeks in combined therapy of 156 patients with viral hepatitis A. In addition to the positive clinico-biochemical effect, these drugs produced an immunomodulatory action and a beneficial effect on the level of blood serum immunoglobulins and the phagocytic activity of peripheral blood neutrophils. Pantetheine provided the most pronounced therapeutic effect.

Administration, Oral↗

[Coa biosynthesis and the structure of its reserve in the liver in mice with diabetes (db/db) after administration of pantothenic acid derivatives].

In the liver of genetically diabetic mice (db/db) a rise of CoA and alterations in the structure of its moiety (an increase in CoA/short-chain fatty acyl-CoA and CoA/long-chain fatty acyl-CoA ratios) were found being one of the hyperlipogenesis-providing factors. A rise of the content of CoA in diabetes was caused by the activation of its biosynthesis from vitamin-containing precursors; an increase in the deposition of the latter in panthotenate-protein complexes was also noted. Panthetine and 4'-phosphopanthotenate administration to diabetic animals returned to normal the level of total and free CoA and the ratios of separate components in the structure of coenzyme moiety, and the content of CoA precursors (phosphopantheteine and dephospho-CoA) in the liver.

Animals↗

[Peculiar features of the effect of cobalamines on the metabolism of vitamin B 12 and pantothenic acid in B 12 deficiency].

A single parenteral administration to B12-deficient rats of cyan cobalamine (CN-Cbl), oxycobalamine (OH-Cbl), methyl cobalamine (CH3-Cbl) and adenosyl cobalamine (Ado-Cbl) at a dose of 100 microgram/kg body weight increased the lowered level of total cobalamines in the liver to reach or exceed the norm. The study of cobalamine-protein complexes (CPC) in the liver of B12-deficient rats showed that the content of free cobalamines and CPC was decreased, the level of CPC degrading at 80 degrees C being particularly low. An administration of OH-Cbl and CH3-Cbl raised significantly the content of CPC degrading at 80 degrees C and presumably containing Ado-Cbl. Under the influence of cobalamines the increased activity of alpha-ketoglutarate dehydrogenase in hepatocytes returned to the normal and the CoA level declined only after administration of CN-Cbl and CH3-Cbl.

Animals↗

Inhibition of rat liver CDPethanolamine: 1,2-diacylglycerol ethanolamine-phosphotransferase activity by ATP and pantothenic acid derivatives.

The properties of rat liver microsomal CDPethanolamine: 1,2-diacylglycerol ethanolamine-phosphotransferase (ethanolaminephosphotransferase; EC 2.7.8.1) are studied with respect to metal ion and substrate concentration. The enzyme requires magnesium (20 mM) or manganese (1 mM) ions for optimum activity. Manganese ions are better activators of ethanolaminephosphotransferase activity than are magnesium ions. Calcium 1 mM) inhibits the magnesium-activated ethanolaminephosphotransferase by 86% and the manganese-activated enzyme by 57%. The Km for CDPethanolamine is 2.4 and 0.7 x 10(-4) M, in the presence of magnesium or manganese ions, respectively. ATP plus pantetheine significantly inhibit the manganese-activated ethanolaminephosphotransferase, while the magnesium-activated enzyme is inhibited by ATP plus pantetheine and slightly stimulated by ATP plus CoA. In the presence of either metal ion, ATP itself inhibits enzyme activity, while CoA or pantetheine when added alone have no effect. Evidence is presented indicating that the inhibition of ethanolaminephosphotransferase activity by ATP plus CoA or ATP plus pantetheine is not due to the formation of acyl-CoA or acyl-S-pantetheine esters. At the present time, however, the true mechanism of inhibition is unknown. The results indicate that the cellular levels of ATP, CoA, pantetheine, magnesium, manganese, and calcium ions may all play a role in the regulation of phosphatidylethanolamine biosynthesis.

Adenosine Triphosphate↗