The effect of hypoxia on oxidative phosphorylation and lipid peroxidation in rat liver mitochondria upon lung inflammation

Hypoxic trainings of rats (maintenance in the test chamber at the "altitude" 4 km above the sea level for 7 hours a day for two weeks) prevent pneumonia-induced activation of peroxidation for lipids of the liver mitochondria. This increases the phosphorylating respiration rate when lipemic serum is used as an oxidation substrate (not succinate). In these experiments the efficiency of oxidative phosphorylation (delta ADP/delta O) when either succinate and glutamate or glutamate and malate have been oxidated corresponded to the values typical of intact animals and was higher when lipemic serum was used. It is supposed that rearrangement of energy reactions of mitochondria is connected with intensification of utilization of lipids and conjugation between their oxidation and phosphorylation. This rearrangement is apparently aimed to prevent the energy deficiency in the organism which arises in patients with pneumonia.     

Effect of heliomycin on the respiration and oxidative phosphorylation of the liver mitochondria of the rat

The effect of heliomycin and known uncouplers of oxidative phosphorylation on respiration and oxidative phosphorylation was studied comparatively. Heliomycin, as well as 2,4-dinitrophenol, valinomycin and gramicidin S inhibited the mitochondrial synthesis of ATP. This process was inhibited completely by heliomycin at a concentration of 1.5 x 10(-5) M. The synthesis of inorganic pyrophosphate, the other macroergic compound, was also inhibited by heliomycin, ATPase and pyrophosphatase of uncoupled mitochondria being not inhibited by the antibiotic. Like 2,4-dinitrophenol, heliomycin stimulated the synthesis of ATPase and respiration in intact mitochondria. Probably, heliomycin inhibited the synthesis of ATP and pyrophosphate by uncoupling the processes of respiration and oxidative phosphorylation. It was shown earlier that heliomycin, a specific inhibitor of bacterial RNA synthesis, also affected energy metabolism of bacterial cells by inhibiting the synthesis of ATP and active transport.     

Inhibition of oxidative phosphorylation and respiration by ozone in tobacco mitochondria

Ozone was found to inhibit oxidative phosphorylation and oxygen uptake in mitochondria of tobacco leaves (Nicotiana tabacum, L. var. White Gold). The inhibition appeared to occur at both substrate and electron-transport chain levels. The inhibition increased with the length of exposure to ozone, however, the phosphorylative system was more sensitive to ozone than the respiratory system. With mitochondria from detached leaves after being treated with ozone at 1 ppm for 1 hour, uncoupling of phosphorylation was demonstrated without any detectable change in the rate of respiration in the early stage of ozone effect. Inhibition of phosphorylation by ozone was also demonstrated in isolated mitochondria without apparent change in optical density of the mitochondrial suspension at 520 mμ. Therefore, mitochondrial swelling appears not to be a necessary first step for ozone-induced uncoupling of phosphorylation. The evidence suggests that inhibition of oxidative phosphorylation in mitochondria may be a primary effect of ozone in tobacco leaves.

Sucrose and glucose, when fed to the detached tobacco leaves before ozone treatment, tended to raise the phosphorylative activity of mitochondria. Mannitol and lactose were less effective.

     

Changes in the SH-group level and respiration during gamma- and Fe2+-induced lipid peroxidation in Ehrlich ascites carcinoma cells

In experiments on Ehrlich ascites tumor cells it was shown that lipid peroxidation induced by gamma-rays and Fe2+ ions was accompanied by a decrease in the endogenous SH-group content at early times after exposure (during 3-hour incubation). It was also established that no significant changes occurred in the oxygen uptake by Ehrlich ascites tumor cells depending on radiation dose of Fe2+ ion concentration. If cells were pre-kept under hypotonic conditions an additional decrease in cell respiration and SH-group content and activation of lipid peroxidation was noted.     

Oxidative phosphorylation in the rat liver mitochondria under activation of lipid peroxidation

The immobilization stress and oxygen effect under pressure of 0.8 atm (hyperbaric oxygenation) considerably activate lipid peroxidation both in the blood serum and rat liver mitochondria. Inhibition and partial separation of oxidative phosphorylation being more pronounced with intensification of lipid peroxidation are simultaneously observed.     

Effects of 5,5'-diphenyl-2-thiohydantoin on respiration and oxidative phosphorylation of rat liver mitochondria.

5,5'-Diphenyl-2-thiohydantoin (DPTH) administered in vitro, inhibited state 3 oxidation, stimulated state 4 oxidation and decreased ADP:O ratio when 3-hydroxybutyrate and succinate were used as substrates. Considerably lower DPTH concentrations were required for the inhibition of 3-hydroxybutyrate oxidation (50% inhibition occurred at approximately 0.17 mumoles DPTH/mg protein) than were needed for inhibition of succinate oxidation (50% inhibition occurred at about 0.62 mumoles DPTH/mg protein). DPTH showed no inhibitory effects when ascorbate plus tetramethylphenylenediamine (TMPD) served as the substrate. The inhibition of state 3 respiration was not reversed by 2,4-dinitrophenol (DNP), although there was a slight increase in the DNP rate:state 3 rate suggesting the presence of a weak DPTH inhibotory site located within the Site I energy transport chain. Uncoupling, in the presence of DPTH, was observed with all substrates. In experiments utilizing sonicated mitochondria, DPTH inhibited NADH-linked oxidation, but did not inhibit succinate or ascorbate plus TMPD oxidation. The effects of DPTH were reversed by dilution and by addition of albumin. DPTH concentrations which produced inhibition of state 3 respiration in vitro were reached, in vivo, in the livers of rats receiving a single oral dose of 40 mg/kg of DPTH.     

Effect of ionizing radiation and Fe2+-induced peroxidation on the lipid phase of erythrocyte membrane preparations

The fluorescent probes, perilene and diphenyl hexatriene, were used to study changes in the lipid phase of erythrocytic ghosts induced by ionizing radiation (100-1000 Gy) and lipid peroxidation initiated by Fe2+ (5-100 microM). Both of the factors were shown to bring about similar changes in the membrane, that is, an increase in the viscosity of the probe localization sites and a decrease in diphenyl hexatriene fluorescence intensity. During the postirradiation incubation of the exposed membranes they were additionally damaged whereas upon peroxidation, most of the changes occurred after 15-min incubation with Fe2+.     

Initiation of nonenzymatic lipid peroxidation in a Fe2+-ascorbate-linolenate system

Using spin trapping method there were discovered and identified the radicals of linolenic acid formed when initiating its peroxidation by the system Fe2+-ascorbate. Mechanism of formation of linolenic acid radicals and their role in initiation of peroxidation were studied. A scheme of reactions of peroxidation initiation in the system Fe2+-ascorbate. linolenic acid is proposed.     

Fuscin,an inhibitor of respiration and oxidative phosphorylation in ox-neck muscle mitochondria

1. The effect of fuscin on the mitochondrial oxidation of pyruvate plus malate, of succinate and of ascorbate plus tetramethyl-p-phenylenediamine (TMPD) and on the redox changes of succinate-reducible cytochromes b and c was investigated using tightly-coupled ox-neck muscle mitochondria.     

Effect of ascorbic acid and oat polyphenols on respiration and oxidative phosphorylation in liver mitochondria in alloxan diabetic rats

30 mg of ascorbic acid and 80 mg of dry oats extracts were administered to rats with alloxan diabetes during a day per 1 kg of live weight. Administration of these preparations during 6, 12 and 24 days prevents the uncoupling action of respiration and oxidative phosphorylation, that was observed in the rats with alloxan diabetes which were not given ascorbic acid and oats polyphenols. The P/O coefficient on the alloxan diabetes rats on the 6, 12 and 24 days was 1.32 +/- 0.027; 1.26 +/- 0.013; 1.22 +/- 0.18, respectively; in the rats which were given ascorbic acid and oats polyphenols to P/O coefficient was 1.85 +/- 0,026, 1.80 +/- 0.024 and 1.75 +/- 0.028, respectively.