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Results for “OXIDATIVE PHOSPHORYLATION”

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PubMed1987

Uncoupling of mitochondrial oxidative phosphorylation by hexetidine.

To gain further insight into the biochemical properties of the antibacterial hexetidine, isolated rat liver mitochondria were added with this drug and investigation made of certain features related to mitochondrial bioenergetics. Hexetidine was found to cause oxidation of intramitochondrial pyridine nucleotides and stimulate the rate of oxygen uptake caused by respiratory substrates involving three, two and one site(s) of phosphorylation. Reversal of oxygen uptake inhibition by oligomycin was also determined. By investigating hexetidine effect on oxidative phosphorylation, hexetidine was found both to inhibit the rate of ATP synthesis and to cause ATP hydrolysis. Likewise, hexetidine capability to produce acidification of extramitochondrial medium and to collapse delta psi was also observed. The reported findings show that hexetidine exhibits uncoupling properties.

Adenosine Triphosphate↗
PubMed1980

[Effect of stenopril on the oxidative phosphorylation processes in rat mitochondria].

The author examined the influence of the preparation stenopryl on the processes of oxidative prosphorilation in the liver and cerebral mitochondria of a rat in view of clarifying some aspects of its pharmacobiochemical mechanism. The results from the experiments in vitro revealed that stenopryl inhibited the processes of oxidative phosphorilation in comparatively high concentrations. The lower concentrations of the preparation did not induce changes. Stenopryl used in vitro, raised ATP-ase activity in liver mitochondria. The data on the experiments in vivo with a dose of 20 mg/kg of stenopryl showed that the preparation did not affect the oxidative processes, when two substrates of oxidation were used, but inhibited phosphorilation when sodium succinate was used. ATP-ase activity during treatment in vivo was not altered.

Adenosine Triphosphatases↗