CONTENT OF CATECHOLAMINES IN BLOOD SERUM OF RATS UNDER FLUORIDE INTOXICATION.

The aim of the research was to determine in the experiment the content of catecholamines in serum of rats exposed to sodium fluoride. The studies were conducted on adult Wistar rats, subjected to oral exposure by means of a probe with aqueous solutions of sodium fluoride (SF) once daily, for 60 days at doses of 1/10, 1/100 and 1/1000 DL50, which correspondingly amounts to 20 mg/kg, 2 mg/kg and 0.2 mg/kg of body weight. Toxification of rats at a dose of 1/100 DL50 for 60 days and at a dose of 1/10 DL50 for 50 days was accompanied by an increase in blood levels of norepinephrine and epinephrine, indicating the hyperactivation of the mediator and hormonal parts of the sympathoadrenal system, and tension of the protective and adaptive reactions of the organism. Prolonged hypercatecholemia may become a pathogenic factor due to intensification of the quinidine route of oxidation of norepinephrine and epinephrine with the formation of reactive radicals and active forms of oxygen. Reduced serum content of catecholamines on the 60th day of oral administration at a dose of 1/10 DL50 reflects, on the one hand, a decrease in their tissue deposit, and, on the other, a decrease in the activity and reserve capacities of the sympathoadrenal system.

NITRIC OXIDE SYNTHESIS INTENSITY ASSESSMENT BY THE CONTENT OF ITS TERMINAL STABLE METABOLITES IN THE BLOOD OF RATS UNDER FLUORIDE INTOXICATION.

The aim of the research was to evaluate the intensity of nitric oxide synthesis in the experiment by the content of its terminal stable metabolites in the blood of rats exposed to sodium fluoride. The studies were conducted on adult Wistar rats weighing 180-220 g, subjected to oral exposure by means of a probe with aqueous solutions of sodium fluoride (SF) daily for 60 days at a dose of 1/10, 1/100 and 1/1000 DL50, respectively, of 20 mg/kg, 2 mg/kg and 0.2 mg/kg body weight. Oral administration of SF to rats at doses of 1/10 and 1/100 of DL50 leads to an increase in blood plasma levels of nitrite and nitrate anions during the first 30 days, indirectly indicating the excessive production of nitric oxide, which in the initial period of intoxication can perform compensatory role, but in the future can cause pathological reactions associated with the activation of oxidative stress. The reduction of nitrite and nitrate anions at the end of the long-term effects of SF indirectly indicates a decrease in the generation of nitric oxide, which may be due, in particular, to the increase in the concentration of peroxynitrite as a result of the use of nitric oxide in reaction with a superoxide anion radical and a deficiency of antioxidant enzymes.

FEATURES OF LIMBIC-NEOCORTICAL AND MONOAMINERGIC CORRELATIONS IN THE DEVELOPMENT OF WITHDRAWAL SYNDROME OF INHALATIONS OF VAPORS OF ORGANIC SOLVENT «646¼ IN RATS.

The aim of the work was to study the limbic-neocortical and monoaminergic features of the development of withdrawal syndrome of volatile organic compounds (VOC) inhalations in rats. The study was carried out in 30 three months old male rats with dependence on inhalations of organic solvent "646" which contains up to 50 % mix of toluene and acetone. It has been shown that the withdrawal syndrome of inhalant is characterized by increased excitability and behavioral manifestations of equivalents of convulsive reactions such as oral hyperkinesis, head shaking and changes in the frequencyamplitude spectrum of the biopotentials in structures of the brain limbic-neocortical system with the initiation in the medial olfactory region and hippocampus. At the hypothalamus level, withdrawal of VOC inhalations produces the depleting impact on the catecholaminergic structures with a stronger effect in neuronal endings with adrenaline as neurotransmitter. Withdrawal syndrome evokes a significant decrease in dopamine content by 61 %, noradrenaline by 77 % and adrenaline by 92 % in the hypothalamus and increase in serotonin concentration in blood serum by 16 % in rats with initial preference to inhalations of organic solvent "646". In rats with the absence of initial preference to inhalations of organic solvent "646" a decrease in adrenaline level in the hypothalamus by 77 % was detected.

Effect of preparations from potentiated ethanol on the content of biogenic monoamines and metabolism of ethanol in tissues of rats during alcoholization.

The effect of homeopathically potentiated ethanol (C30 and C200) on ethanol metabolism was studied in alcoholized rats. We measured ethanol concentration in the blood, alcohol dehydrogenase activity in the liver, and contents of biogenic monoamines in the hypothalamus, septum, and whole blood. Potentiated preparations of ethanol were efficient after long-term treatment and delayed ethanol elimination from the blood. Preparation C200 increased alcohol dehydrogenase activity. Potentiated preparations of ethanol (particularly C200) produced a positive effect on catecholaminergic and serotoninergic systems of the brain, i.e. they enhanced protective and adaptive reactions.

Effects of potentiated antibodies against brain-specific S100 protein on biogenic amine content and lipid peroxidation in rats under conditions of alcoholization.

Antibodies against S100 protein in ultralow doses specifically affected catecholamine metabolism in rats withdrawn from chronic ethanol exposure. The contents of tryptophan, tyrosine, and norepinephrine in brain structures returned to normal. The concentrations of dopamine, epinephrine, and norepinephrine in the peripheral blood decreased. Modulation of monoamine content in the peripheral blood suggests that antibodies against S100 protein possess stress-protective activity during ethanol withdrawal.

Potentiated antibodies against morphine: effects on biogenic amines and lipid peroxidation in chronically morphinized rats.

The efficiency of potentiated antibodies against morphine was studied on the model of chronic morphine intoxication. Test antibodies stimulated catecholamine metabolism in the hypothalamus (i.e., prevented initiation of catecholamine- and histaminergic peripheral reactions) and normalized lipid peroxidation.