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Results for “OXIDATIVE PHOSPHORYLATION”

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PubMed1988

Enhanced oxidative phosphorylation in rat liver mitochondria following prolonged in vivo treatment with imipramine.

1. Effects of prolonged in vivo administration of the tricyclic antidepressant drug imipramine on oxidative energy metabolism in rat liver mitochondria were examined. 2. Imipramine treatment resulted in an increase in state 3 respiration rates with all the substrates tested as early as one week after treatment; this was sustained through the second week of treatment. 3. The changes in respiration rates were accompanied by a selective increase in the intramitochondrial cytochrome aa3 and c + c1 contents after both one and two weeks of treatment. 4. Administration of imipramine did not alter the total liver protein content per g tissue, the mitochondrial protein content per g tissue or the mitochondrial yield. 5. Kinetic analyses of succinoxidase activity in terms of Arrhenius plots indicated possible alterations in mitochondrial membrane lipid milieu and membrane fluidity after the drug treatment, especially in the second week.

3-Hydroxybutyric Acid↗
PubMed1985

Multiple relationships between rate of oxidative phosphorylation and delta microH in rat liver mitochondria.

The relationship between rate of ATP synthesis and transmembrane electrochemical proton gradient has been determined in rat liver mitochondria oxidizing succinate, using the respiratory inhibitor malonate or the uncoupler FCCP to decrease delta microH progressively. As previously reported [(1982) Eur. J. Biochem. 126, 443-451] two different relationships are obtained depending on the method used. Evidence is presented that this result is not due to underestimation of the delta microH maintained by fast-respiring mitochondria, as recently suggested [(1985) FEBS Lett. 181, 323-327].

Adenosine Triphosphate↗
PubMed1977

[Effects of methylcyclopentadienyl manganese tricarbonyl (MMT) of rat liver mitochondria. I. Effects, in vitro, on the oxidative phosphorylation (author's transl)].

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an effective inhibitor of mitochondrial respiration associated with NAD+-linked substrates. At concentrations which inhibit glutamate-malate oxidation (over 80% inhibition) succinate and tetramethylphenylenediamine (TMPD)-ascorbate are inhibited less than 25%. MMT inhibits both electron and energy transfer in mitochondria as revealed by the partial release of MMT inhibition by 2,4-dinitrophenol (DNP). The data indicated that the effects of MMT are supported by energy conservation at site I of the respiratory chain.

Animals↗