Argocytes containing enzyme nanoparticles reduce toxic concentrations of arginine in the blood.

A method for incorporation of arginase nanoparticles into mouse erythrocytes has been developed and the possibility of reducing blood arginine concentration in animals with experimental hyperargininemia with arginase-loaded erythrocytes (argocytes) has been studied. Argocyte infusion to animals with hyperargininemia led to a rapid decrease in blood arginine concentration within 1 h and this effect of argocytes persisted for at least 4 h. This was paralleled by an increase in plasma concentrations of urea and ornithine. Hence, plasma arginine is hydrolyzed by arginase incorporated into argocytes; argocytes are functionally active and can serve as a defense system in pathological hyperargininemia, while the method developed by us can be regarded as a new nanobiotechnology for medicine and veterinary.

Experiments on alcocytes containing enzyme nanoparticles for reducing toxic blood concentration of ethanol.

We developed a method of introduction of alcohol dehydrogenase and aldehyde dehydrogenase into mouse and human erythrocytes. The possibility of using erythrocytes loaded with the two enzymes (alcocytes) for reducing ethanol concentration in animal blood was studied. Injection of alcocytes to mice led to accelerated decrease in ethanol concentration as soon as after 5 min and this capacity of alcocytes persisted for at least 2 h. Alcocytes prepared from fresh or preserved human blood did not survive in mice. Thus autologous alcocytes is functionally active and can be used as a protective system in acute alcohol intoxication. The developed method can be regarded as a new medical biotechnology.

Activation of AMP deaminase and adenosine deaminase in the liver during ammonia poisoning and hepatitis.

We studied the effect of acute ammonia poisoning and CCl4-induced subacute hepatitis on activities of AMP deaminase and adenosine deaminase in rat liver. Both models of liver failure were accompanied by an increase in activities of AMP deaminase and adenosine deaminase in the cytoplasmic fraction of the liver (by 2.4-4.2 times compared to the control). A direct correlation was found between activities of AMP deaminase and adenosine deaminase. We believe that two parallel pathways of AMP degradation are activated simultaneously, which leads to rapid depletion of adenylate reserves under pathological conditions.

Studies on ammocytes: development, metabolic characteristics, and detoxication of ammonium.

The possibility of reducing ammonium concentration in the blood of mice with hyperammonemia with ammocytes (erythrocytes loaded with glutamate synthase) and the metabolic characteristics of these cells were studied. Injection of ammocytes into the blood stream of animals with hyperammonemia led to reduction of the blood ammonium concentration within the first 30-120 min and this activity of ammocytes was retained for at least 2 days. Endogenous phosphofructokinase, glucose-6-phosphate dehydrogenase, hexokinase, lactate dehydrogenase, pyruvate kinase, and Na(+),K(+)-ATPase in ammocytes remained at the levels of catalytic activities characteristic of intact erythrocytes. Hence, ammocytes are functionally active cells and can be used as a protective system in pathological hyperammonemia, while the method can be regarded as a new technology for medicine and veterinary.

Effects of hydrated forms of C60 fullerene on amyloid 1-peptide fibrillization in vitro and performance of the cognitive task.

It has been shown for the first time by transmission electron microscopy that the hydrated fullerene C60 inhibited the fibrillization of amyloid-beta25-35 peptide. The fullerene affected the amyloid-beta25-35 assembly, manifesting its anti-amyloidogenic capacity. Our in vivo investigations demonstrated also that a single intracerebroventricular injection of the C60 hydrated fullerene at a dose of 7.2 nmol/ventricle significantly improved the performance of the cognitive task in control rats. The intracerebroventricular injection of the C60 hydrated fullerene (3.6 nmol/ventricle) prevented the impairment of performance of the cognitive task induced by amyloid-beta25-35 (22.5 nmol/ventricle). The results obtained may be useful in the development of therapy of Alzheimer's disease.