[Energy regulation of transmembrane potentials in liver cells during hypoxia]. / Energeticheskaia reguliatsiia transmembrannykh potentsialov kletok pecheni pri gipoksii.

The influence of oxygen tension on values of transmembrane potentials in rat liver cell was investigated. The membrane potential was assessed by the uptake TPP as was determined on the ion-selective electrode. Infusion of inhibitors oxidative phosphorylation and glycolysis to incubation medium caused depolarization on the mitochondrial, and, the plasma membranes of this cell. These and other experimental results suggest that there is an interaction between mitochondrial and cytosol pools of ATP, which determine steady-state values on transmembrane potential liver cell under hypoxia.

[Effects of emotional-pain stress on induction of P-450 cytochrome in the rat liver]. / Vliianie émotsional'no-bolevogo stressa na induktsiiu tsitokhroma P-450 v pecheni krys.

Stress effect on cytochrome P-450 content in rat liver has been studied. There is evidence to the effect that stress factors of different origin cause the decline in cytochrome P-450 content both in the control group and in the conditions of induction. The data obtained enable us to suppose that stress causes intensification of cytochrome P-540 degradation process, the induction efficiency being steady.

[Hydroxylation products of hydrophobic xenobiotics--stabilizers of cytochrome P-450 in the hepatocytes]. / Produkty gidroksilirovaniia gidrofobnykh ksenobiotikov--stabilizatory tsitokhroma P-450 v gepatotsitakh.

The effects of the hydroxylation product 3,4-benzo(a)pyrene and the free radical scavenger 1,2,3-trioxybenzene on cytochrome P-450 degradation in isolated rat hepatocytes induced by the Fe2+-ADP + NADPH system activating lipid peroxidation (LPO) were investigated. During incubation of hepatocytes, cytochrome P-450 is destroyed due to accumulation of LPO products. Addition of the free radical scavenger 1,2,3-trioxybenzene and the monoxygenase substrate 3,4-benzo(a)pyrene to the incubation medium induces inhibition of LPO and simultaneous stabilization of cytochrome P-450. Deceleration of malonic dialdehyde production by the free radical scavenger of the monoxygenase substrate suggests that both the compounds stabilize cytochrome P-450. It is assumed that in liver hepatocytes, exogenous free radical scavengers of the phenolic type and the products of their decarboxylation protect cytochrome P-450 against the LPO-induced destruction via oxidative metabolism of hydrophobic substrates.

[Antioxidants as stabilizers of cytochrome P-450 in hepatocytes]. / Antioksidanty kak stabilizatory tsitokhroma P-450 v gepatotsitakh.

Spontaneous destruction of cytochrome P-450 arising from activation of lipid peroxidation (LPO) occurs during incubation of hepatocytes. LPO activation in hepatocyte suspension by a catalytic system containing Fe2+--ADP plus NADP X H makes the destruction of cytochrome P-450 more rapid. Supplementation of the incubation medium with the antioxidant, 2-ethyl-6-methyl-3-hydroxypyridine (HP-6), inhibits LPO, on the one hand, and stabilizes cytochrome P-450, on the other one. Ionol appeared to be a more effective LPO inhibitor in hepatocytes and, accordingly, a more effective stabilizer of cytochrome P-450 than water-soluble HP-6.

[Morphologic, electrophysiologic and metabolic indices of cerebellar neuron functioning in tissue culture]. / Morfologicheskie, élektrofiziologicheskie i metabolicheskie pokazateli neironov mozzhechka v usloviiakh kul'tury tkani.

A comparative investigation of morphological, electrophisiological and metabolic indices of the functioning of cerebellar neurons developing in vivo and in conditions of the organotypical culture permitted us to distinguish a period (20--25 days) when properties of the culture of nervous tissue most resemble the characteristics of the brain of adult animals. Cultivated nervous tissue may be used as a model for studies of fine mechanisms of the nervous system functioning in the ontogenesis.