Humus state and nitrogen stock of basic types of soil exposed to lasting fertilization

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The effect of dithiocarbamates on neurotoxic action of 1-methyl-4- phenyl-1,2,3,6 tetrahydropyridine (MPTP) and on mitochondrial respiration chain

The neurotoxin MPTP induces in human and in some laboratory animals parkinsonism-like neurological disorder, biochemically characterized by selective and irreversible decrease of dopamine content in striatum. The terminal step in the mechanism of neurotoxic action of MPTP is the inhibition of mitochondrial respiratory chain by pyridinium metabolite (MPP+) resulting in energy depletion and nervous cells death. Earlier it was shown that some chemical compounds, in particular diethyldithiocarbamate (DTC), can potentiate MPTP neurotoxicity. In the present work we have studied the influence of DTC derivatives on MPTP neurotoxic effect in vive and on MPP+ inhibition of mitochondrial respiration (both on intact mitochondria and on submitochondrial particles) in vitro. It was revealed that DTC alone change mitochondrial membrane state by respiratory chain uncoupling and inhibition. DTC and MPP+ mutually potentiate inhibition of electron transport as well. The combined effect of DTC plus MPP+ action on mitochondria respiration reflects the sum of reciprocally leveling and potentiating factors and can explain the order of efficacy of MPTP-neurotoxicity potentiation in vive in series of close DTC derivatives.</p

Effect of potassium chloride and actovegin infusions on cardiohemodynamics and enzymemia in acute period of myocardial infarction among patients with left ventricular systolic dysfunction

То investigate effect of potassium chloride and its combination with actovegin infusions on cardiohemodynamics and CK, AsAT, myoglobine levels in AMI associated with left ventricular systolic dysfunction, two groups of patients were examined. Participants from the first group (n=26) received infusions of 1 % potassium chloride (4-6 g/d). In the second group, patients (n=23) received infusions of 1 % potassium chloride plus actovegin (0. 15-0. 3 mg/kg/h; 160-320mg/d). Comparative analysis of the data obtained revealed that, after infusion of potassium chloride plus actovegin (0. 15-0. 3 mg/kg/h), left ventriclar volumes reduced, IV contractility improved, BP and cardiac output increased, together with decrease in CVP, HR, DP (double product), and CK activity

The effect of dithiocarbamates on neurotoxic action of 1-methyl-4- phenyl-1,2,3,6 tetrahydropyridine (MPTP) and on mitochondrial respiration chain

The neurotoxin MPTP induces in human and in some laboratory animals parkinsonism-like neurological disorder, biochemically characterized by selective and irreversible decrease of dopamine content in striatum. The terminal step in the mechanism of neurotoxic action of MPTP is the inhibition of mitochondrial respiratory chain by pyridinium metabolite (MPP+) resulting in energy depletion and nervous cells death. Earlier it was shown that some chemical compounds, in particular diethyldithiocarbamate (DTC), can potentiate MPTP neurotoxicity. In the present work we have studied the influence of DTC derivatives on MPTP neurotoxic effect in vive and on MPP+ inhibition of mitochondrial respiration (both on intact mitochondria and on submitochondrial particles) in vitro. It was revealed that DTC alone change mitochondrial membrane state by respiratory chain uncoupling and inhibition. DTC and MPP+ mutually potentiate inhibition of electron transport as well. The combined effect of DTC plus MPP+ action on mitochondria respiration reflects the sum of reciprocally leveling and potentiating factors and can explain the order of efficacy of MPTP-neurotoxicity potentiation in vive in series of close DTC derivatives.</p