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Biotin (0.3 mg/kg per os) and ubiquinone Q10 (50 mg/kg, per os) during chronic administration were found to produce stimulating effects on premature animals. The two drugs contributed to a more rapid development of memory and learning processes in premature new-born rats than in mature ones, normalized the major parameters of carbohydrate and lipid metabolism. Some specific features and differences were ascertained in the stimulating effects of biotin and ubiquinone Q10.

Anticonflict and antiamnestic effects of original D,L-carnitine chloride have been studied. By using a model of electroshock amnesia, carnitine chloride showed a pronounced antiamnestic effects, by positively affecting the behaviour of animals exposed to a conflict situation. The neuropharmacological effects of carnitine chloride have been found to be implicated in the metabolism of proteins and lipids.

Coenzyme A disulfide (CoA disulfide) was pharmacologically studied. It has been found to normalize lipid and carbohydrate metabolism when given in a dose of 2 mg/kg, i.m., in diverse liver dysfunctions. It possesses an antihypoxic action under hemic and histotoxic hypoxia. When given in small doses (80-160 micrograms/kg, i.v.), CoA disulfide depresses the function of cellular hemostasis.

Psychotropic activity of different salts of homopantothenic acid was studied. In homopantothenic acid derivatives, the substitution of calcium ions by sodium and magnesium ions gives rise to a decrease of the sedative and potentiation of the stimulating properties.

D, L-carnitine chloride antihypoxic action was studied. Carnitine chloride (100-200 mg/kg) was found to increase mouse life expectancy under different experimental models of hypoxia both at acute and chronic administration.

It has been shown in experiments on rats that daily administration of methylcobalamine in a dose of 50 micrograms/100 g bw produces marked activation of the regeneration of mechanically damaged axons of motoneurons. Systematic administration of the drug has a protective action on the development of neuromuscular transmission blockade induced by botulinum toxoid.

Experiments on albino mice and rats have shown that pantogam, a derivative of pantothenic acid, potentiates the hypnotic effects of hexobarbital and barbital and enhances the effect of subthreshold doses of hexobarbital. The drug inhibits the amphetamine action in the amphetamine hyperaction test without affecting hexobarbital and amphetamine metabolism, or without increasing the blood-brain barrier permeability for these compounds and barbital. Pantogam does not influence the intensity of ethylmorphine N-demethylation in liver homogenates and the content of cytochrome P 450 and b5 in liver microsomes.

Single administration of 0.25 microgram of sunthetic Ialpha-hydroxycholecalciferol (IalphaOHD3) into nephrectomized rats, maintained at D-avitaminous diet, improved the active transport of calcium ions against the concentration gradient in small intestine of these animals, whereas ergocalciferol was biologically inactive under the same conditions. Administration of IalphaOHD3 during 5 days at a dose 0.025 microgram normalized calcium content in blood serum of rats with D-avitaminosis, Increased doses of IalphaOHD3, administered into intact animals, caused transient hyperphosphatemia, hypercalcemia, calcinosis of internal tissues (kidney heart, aorta) as well as death of some animals. IalphaOHD3 exceeded 400-fold the hypercalcemic and calcinose effects of ergocalciferol. LD50 for IalphaOHD3 was equal to 100 microgram/kg, if it was administered during 5 days per os. Tissue calcinosis was developed after administration of a daily dose 10 microgram/kg, moderate hypercalcemia was caused by a daily dose 1 microgram/kg or 0.25 microgram per an animal; this amount is only 10-fold higher as compared with the physiologic requirement. Ergocalciferol caused hypercalcemia and metastatic calcification only at a dose 4000 microgram/kg. Clinical use of IalphaOHD3 at doses, exceeding the physiologic requirements, has to be prohibited due to high activity of the preparation and to toxicity of its increased doses.

In white rats with B6-avitaminosis, the B6-vitamin activity of pyridoxal-phosphate and of pyridoxine was studied in their epicutaneous and peroral application. It is revealed that pyridoxal-phosphate in epicutaneous application displays more activity than pyridoxine and pyridoxal-phosphate applied perorally. Pyridoxine in epicutaneous application does not reveal the B6-vitamin activity.

The effect of a single and 2-week administration of ubiquinone-9 on the blood coagulation system and the functional activity of platelets was studied in the experiments in vitro and in vivo on rats. It was shown that a single dose of 150 mg/kg of ubiquinone decreased adhesion and that of 5 mg/kg decreased aggregation of platelets. Both with a single and 2-week drug administration in doses of 5, 50 and 150 mg/kg an insignificant decrease of coagulability was observed.

Intraperitoneal administration of disulphide pyridoxine (pyriditol) to albino mice in a dose of 300 mg/kg brings down the GABA level and the GABA-transaminase activity in the brain, the glutamic acid content and the glutamate-decarboxylase activity remaining unchanged. In the liver and, especially, in the kidneys of test animals the activity of aspartate-and alanine-aminotransferase goes down. The diurnal urinary output of the animals shows a decreased passage of 4-pyridoxic acid. These results are interpreted to be consequent upon the antivitamin action of pyriditol with respect to pyridoxine.

The effect of potassium orotate in a dose of 100 mg/kg and sodium uridine monophosphate (UMP) in doses of 25, 50 and 100 mg/kg on the development of adrenaline myocardiodystrophy was studied in experiments on white rats. Preliminary administration of these drugs increases the animals' resistance to the adrenaline-induced necrotic affection of the heart. It has been noted that the animals' survival increased and the cardiac muscle status improved (according to ECG readings, biochemical findings and relative heart weight). Administration of UMP in doses of 50 and 100 mg/kg exerted a more pronounced beneficial prophylactic effect as compared with potassium orotate.

Leucovorin and cobamamide administered alone and in combination potentiate the proliferative activity of the erythroid and myeloid cells of the bone marrow. There is lack in mutual potentiation of the drugs.

Experiments on rats were made to study membrane potentials (MP) of secretory cells of the salivary glands, the content of biogenic amines and lactate dehydrogenase (LDH) isozymes of the salivary gland tissue in trauma after pretreatment with methylcobalamine. Twenty-four hours after trauma the salivary gland showed a decrease in the content of LDH aerobic fractions, the lowering of noradrenaline concentration with no changes in the MP of glandular cells outside the zone of injury. Administration of cobalamine did not cause any changes in the parameters under study. There was an increase in the polarization level of acinar and duct cells, normalization of noradrenaline content, and a rise of adrenalin concentration with persistent reduction in aerobic fractions of LDH in salivary gland trauma after pretreatment with methylcobalamine. It is concluded that methylcobalamine administration may have a therapeutic effect in salivary gland trauma.

The experiments on rats showed that cobamamide (0.5 mg/kg) and leukovorin (5 mg/kg) administered daily exerted a pronounced activating effect on the process of regeneration of mechanically injured nerve trunks. The combined administration of the drugs fails to potentiate the effect of each drug on the process of the skeletal muscle reinnervation.

Pyriditol (encephabol, enerobol, pyrithioxin, etc.), a disulfide derivative of pyridoxin, exerts an inhibitory effect on hexobarbital and amphetamine metabolism i vivo and on ethylmorphine N-demethylation in vitro. In the latter case the inhibition proceeds according to the mixed type of action. Pyriditol potentiates the hypnotic action of hexobarbital and barbital as well as the effects of amphetamine stereotypy. The mechanism of the potentiating of hexobarbital and amphetamine effects is of combined character and is conditioned both by the physiological properties of pyriditol and its inhibitory effect on hexobarbital and amphetamine metabolism.

The antihypoxic properties of GABA-containing vitamin derivatives (pyridoxalphosphate-GABA, picamilone, pantogam, sodium homopantothenate) as compared with GABA were studied. All agents were found to increase mouse life expectancy under hypoxia in contrast to GABA.