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N K Segal'

Publications and source records attributed to N K Segal'.

5 recordsLinked to original sources
PubMed1993

[The effect of inhibitors of the Q-cycle on cyano-resistant oxidation of malate by rat liver mitochondria in the presence of menadione].

Based on the inhibitor analysis data, it has been assumed that the Q-cycle plays a role in the cyano-resistant malate oxidation induced by menadione (90 microM) in rat liver mitochondria. The extent of involvement of Q-cycle transmitters in the cyano-resistant respiration of mitochondria is determined by the mode of the electron supply into the Q-cycle. In the presence of dicumarol, i.e., under conditions when CoQ and menadione are reduced by NADH-quinone reductase, the bulk of the electrons pass through the o-center of the Q-cycle. Myxothiazole inhibits the respiration by 70-80%, while antimycin--by only 20-30%. In the presence of myxothiazole and antimycin menadione oxidizes cytochrome b. In the presence of rotenone, when menadione is reduced by DT-diaphorase, the rate of cyano-resistant respiration decreases approximately twofold; its sensitivity towards myxothiazole and antimycin drops down to 40%. In the absence of rotenone and dicumarol the Q-cycle does not participate in the cyano-resistant respiration which under these conditions is insensitive either to myxothiazole or to antimycin. It is concluded that the mechanism of cyano-resistant respiration changes with an alteration in the rates of quinones K3 and CoQ reduction. The mechanism of cyano-resistant respiration is also controlled by the medium tonicity. A reduction in the medium tonicity decrease the participation of the Q-cycle and, correspondingly, the sensitivity of the cyano-resistant respiration towards myxothiazole and antimycin.

Animals↗
PubMed1993

[Mitochondrial proteolipids].

A convenient procedure is proposed for extracting mitochondrial proteolipids using a single phase mixture chloroform-methanol-water (1:2:0.8 v/v) with subsequent separation of the phases. The proteolipids were concentrated at the interface between the phases and thus purified from the bulk of the phospholipids. It was found that the mitochondrial proteolipids represent stable complexes of phospholipids with some low molecular weight proteins (M(r) = 7-18 kDa). The latter are destroyed at acid pH values. The phospholipid/protein ratio was found to be equal to 6 (assuming the molecular masses of the proteins and phospholipids to be equal to 10 and 0.8 kDa, respectively). The phospholipid composition of the tightly bound proteolipids thus obtained did not differ from that of the mitochondrial phospholipids. Using 31P-NMR, nonbilayer structures were found to arise from proteolipid reconstitution into multibilayer liposomes.

Animals↗
PubMedDate not supplied

[The energy metabolism of the liver under the action on the body of different durations of hypokinesia].

Studies of tissue respiration and oxidative phosphorylation of homogenates in the liver of white rats indicated that the 3-day hypokinesia is associated with a decreased rate of endogenic respiration and an increased amythal-resistant respiration. On the 10th day, there occurs a sharp increase of the oxidation rate of the endo- and exogenic substrates and the separation of oxidative phosphorylation takes place. During 30-day immobilization, the homogenate respiratory activity again decreases while on the 70-140th days of an exposure the oxidation rate of endo- and exogenic substrates increases with an increased effect of endogenic succinate on the hepatocyte energy metabolism. The possible mechanism disturbances in the liver of immobilized animals are discussed.

Animals↗
PubMedDate not supplied

[Energy metabolism in the kidneys after hypokinesia of varying duration].

This paper presents data suggesting that tissue homogenates can be used to assess mitochondrial oxidation. The effect of hypokinesia of various duration on tissue respiration and oxidative phosphorylation of rat kidneys was investigated for the first time. It was found that 3-day hypokinesia led to a decrease of tissue respiration due to a lower contribution of endogenous fatty acids; 10-day hypokinesia caused activation of tissue respiration on endogenous and exogenous pyridine and flavoprotein-dependent substrates; 30-, 70- and 140-day hypokinesia brought about changes in energy formation at the expense of inhibition of respiratory activity of preparations and uncoupling of oxidative phosphorylation. Mechanisms of the above disturbances in energy metabolism reactions of kidneys are discussed.

Animals↗