[AMP deaminase activity in hyperoxia and the effect of AMP on animal sensitivity to oxygen under pressure].

Under the effects of 0.7 MPa of oxygen leading to a convulsive state, AMP-deaminase activity increased significantly in the rat brain mitochondrial fraction with only a tendency to increase in cytoplasmic fraction. Stimulated effects of the enzyme allosteric activator ATP is more obvious in intact animals than in hyperoxic ones.

[Glucose-6-phosphate dehydrogenase activity in rat serum in hyperoxia, hypoxia, and cooling].

Activity of glucose-6-phosphate dehydrogenase (G6PD) was increased in blood serum in hypoxic hypoxia, hypoxia and cooling stress. The degree of this alteration depended on duration of the action of the effectors and on oxygen pressure. Adaptation to cooling was characterized by stabilization of enzymatic activity at the new metabolic step.

[Monoamine oxidase activity in the brain during adaptation to cold and simultaneous exposure to cold and hyperbaric oxygenation].

One--day cold exposure decreases the monoamine oxidase type A activity by 52--54% (serotonin and noradrenaline substrates); the monoamine oxidase type B activity by 14%. Three--day cold exposure leaves the monoamine oxidase type B activity unchanged and decreases the monoamine oxidase type A activity by 29--32%; the enzyme of the latter type acquires the ability for deamination of glucosamine, putrescine and GABA. Under cold adaptation (45 days, 2 degrees C) the monoamine oxidase type A activity remains reduced as on the 3rd day, the type B activity decreases by 19%; enzyme substrate specificity does not change at all.

[Effect of low temperature on monoamine oxidase and substrate specificity in the mitochondrial fraction of rat brain].

Maintenance of animals for three days at 2 degrees C produces changes in the substrate specificity of type I monoamine oxidase (MAO). These changes manifest in serotonin and noradrenaline deamination and in a several-times increase in deamination of glucosamine, putrescine and gamma-aminobutyric acid. The cold-induced increase in AMP deamination is not related to MAE.

[Noradrenaline concentration and monoamine oxidase activity in regions of the brain and the livers of hyperoxic rats].

Content of noradrenaline and the activity of mitochondrial monoamineoxidase (MAO) were studied in cerebral cortex, hypothalamus, mesencephalon, medulla oblongata and liver tissue after the oxygen treatment under pressure (4 atm) within 1 hr. Content of noradrenaline was decreased in all the brain and liver tissues studied. The most distinct decrease was found in hypothalamus and the less marked one -- in liver tissue.

[Possible change in the substrate specificity of the monoamine oxidase of rat brain and liver mitochondria in hyperoxia].

Maintenance of animals in conditions of increased oxygen pressure at 4 atm within 1 h caused a decrease in activity of monoamine oxidase from rat brain mitochondria and liver tissue; at the same time, deamination of putrescine and AMP was increased. Deamination of glucosamine was also observed in brain mitochondria. The qualitative alterations in the monoamine oxidase activity were more distinct in brain than in liver tissue.

[ATPase activity of subcellular rat brain fractions following hyperoxia].

The total Mg2+-ATPase and Na+, K+-ATPase activity was studied in the fractions of "400 g X for 20 min" and "900 g X for 30 min" conditionally called the fraction of the external cellular membranes and total fraction of mitochondria. The subcellular fractions were isolated from great hemispheres and stem part of the rat brain. The brain of control animals and those during a severe spasmodic attact induced by the oxygen action at a pressure of 6 ati was studied.

[Monamine oxidase activity of the brain and liver mitochondria under the action of high-pressure oxygen on animals].

The monoamine oxidase (MAO) activity with tryptamine, 5-hydroxytryptamine and noreponephrine as substrates was studied as affected by different conditions of hyperbaric oxygenation. Exposure of rats to oxygenation at 1 ati resulted in a 75% activation of the brain mitochondria. MAO activity with norepinephrine and in an insignificant increase in the activity with the other substrates.