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Experimental encephalopathy induced by intoxication with 4-pentenoic acid, an inhibitor of β-oxidation of fatty acids, is accompanied by suppression of succinate-and NAD-dependent oxidative pathways in brain mitochondria, uncoupling of oxidative phosphorylation, and activation of LPO. Deenergization of mitochondria and LPO progressed 14 days after discontinuation of 4-pentenoic acid injections. In experimental encephalopathy, hepatoprotective agent Eplir containing essential phospholipids improves coupling of oxidative phosphorylation and energization in mitochondria and inhibits LPO.

After long-term adaptation to intermittent hypoxia, rats with an initially low resistance to acute oxygen deficiency were 2 to 4 times more resistant to it, while highly resistant rats did not show a significant change in resistance. The adaptation was accompanied by weakening of the electron-transporting function of the respiratory chain and increasing efficiency of oxidative phosphorylation in the brain mitochondria oxidizing NAD-dependent substrates, indicating that energy was produced in a more economical way. The succinate oxidase pathway of oxidation was found to be utilized to only a limited extent as a compensatory mechanism in animals exposed to intermittent hypoxia over a prolonged period. The effects of adaptation were more marked in the brain mitochondria of rats initially highly sensitive to oxygen deficiency.

Posthypoxic encephalopathy is characterized by inhibition of the succinate oxidase stage in cerebral energy production. When administered to rats exposed to hypoxia,Bergeniae crassifolia extract reduced mortality and restricted the inhibition of rapid metabolic cluster reactions.

Inin vitro experiments, antineoplastic anthracycline antibiotic doxorubicine caused deenergization of rat brain mitochondria due to oxidation-phosphorylation uncoupling and inhibition of succinate oxidase system. Reduced production and oxidation of succinic acid is the most early effect of doxorubicin on mitochondrial oxidation.

Changes in NADH fluorescence in brain mitochondria of rats exposed to hypercapnic hypoxia were studied. The status of the succinate oxidation system determines the level and kinetic characteristics of pyridine nucleotide reduction. The kinetic characteristics of energy production are more susceptible to hypoxia than changes in NADH level.

In rats with experimental encephalopathy caused by intoxication with 4-pentenoic acid inhibiting beta-oxidation of medium- and long-chain fatty acids, hepatoprotector silimarin inhibited LPO, prevented deenergization and maintained high respiratory activity of brain mitochondria, and increased the rate and coupling of oxidation and phosphorylation. Succinic acid improved oxidation of substrates in motochondria and promoted activation of succinate-dependent ATP generation. Silimarin and succinic acid used together produced a synergistic protective effect on brain mitochondria surpassing the protective effects of individual preparations and prevented LPO activation.

Cerebronorm prevents de-energization of mitochondria, limitation of succinate- and NAD-dependent energy production, and oxidation-phosphorylation uncoupling and inhibits LPO processes in the brain of rats under conditions of hypoxia.

The effects of inhibition of ubiquinols and ubiquinones with various length of isoprenoid chain on the lipid peroxidation in membranes of brain mitochondria and synaptosomes were studied. The efficiency of inhibition effects of ubiquinols depends on the length of isoprenoid chain. Ubiquinols with shorter isoprenoid chains demonstrated more effective inhibition.

An electron-cytochemical investigation was made of oxidation of 3,3′-diaminobenzidine (DAB) in the brain of rats and man at different times after death. The oxidation product of DAB was localized in the mitochondria, lipofuscin granules, and erythrocytes. Oxidation of DAB by rat and human brain mitochondria was shown to be only very slightly depressed even 2 days after death.