Pyruvate transport by thermogenic-tissue mitochondria

Proudlove, Michael O.; Beechey, R. B.; Moore, Anthony L.

doi:10.1042/bj2470441

Cited by 23 publications

(22 citation statements)

References 18 publications

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“…In this study we showed that MPC can also be inhibited by Zaprinast. Inhibition or knockdown of MPC prevents pyruvate-dependent acetyl-CoA formation and O 2 consumption (5,6,42) and decreases the lactate/pyruvate ratio (43). Our study shows that Zaprinast and UK5099 not only block pyruvate-dependent mitochondrial O 2 consumption and citrate synthesis in brain mitochondria but also cause increases in pyruvate and aspartate and decrease in glutamate in brain mitochondria and the retina.…”

Section: The Effect Of Zaprinast On Glutamate and Aspartate Occurs Inmentioning

confidence: 63%

Inhibition of Mitochondrial Pyruvate Transport by Zaprinast Causes Massive Accumulation of Aspartate at the Expense of Glutamate in the Retina

Cleghorn

Contreras

et al. 2013

Journal of Biological Chemistry

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Background: Pyruvate transport into mitochondria is a key step in energy metabolism. Zaprinast is a well known phosphodiesterase inhibitor.Results: Zaprinast has a strong influence on pyruvate transport into mitochondria. Conclusion: Inhibition of the mitochondrial pyruvate carrier by Zaprinast causes accumulation of aspartate at the expense of glutamate. Significance: Maintenance of normal amino acid levels in the retina relies on pyruvate transport into mitochondria.

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Section: The Effect Of Zaprinast On Glutamate and Aspartate Occurs Inmentioning

confidence: 63%

Inhibition of Mitochondrial Pyruvate Transport by Zaprinast Causes Massive Accumulation of Aspartate at the Expense of Glutamate in the Retina

Cleghorn

Contreras

et al. 2013

Journal of Biological Chemistry

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“…maculutum were prepared as described by Proudlove et al (1987) and purified on a 21% (v/v) self-generating Percoll gradient as previously described (Moore et al, 1993a).…”

Section: Lsolation Of Mitochondriamentioning

confidence: 99%

Developmental Regulation of Respiratory Activity in Pea Leaves

Lennon

Pratt²,

Leach³

et al. 1995

Plant Physiol.

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“…The (26). The proportion of lipophilic ion accumulated free to respond to the mitochondrial membrane potential was calculated from the ratio of observed Rb+ distribution to that of TPMP+.…”

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confidence: 99%

Role of Nonohmicity in the Regulation of Electron Transport in Plant Mitochondria

Whitehouse¹,

Fricaud²,

Moore³

1989

Plant Physiol.

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The relationship between the respiratory rate and the membrane ionic current on the protonmotive force has been investigated in percoll purified potato mitochondria. The dependence of the membrane ionic current on the membrane potential was monitored using a methyltriphenylphosphonium-sensitive electrode and determining the maximal net rate of depolarization following the addition of a respiratory inhibitor. We have confirmed that a nonohmic relationship exists between the ionic conductance and membrane potential. Addition of ATPase inhibitors markedly increased the initial rate of dissipation suggesting that in their absence the dissipation rate induced by respiratory inhibitors is partially offset by H+-efflux due to the hydrolysis of endogenous ATP. This was corroborated by direct measurement of endogenous ATP levels which decreased significantly following dissipation of the membrane potential. Results are discussed in terms of the regulation of electron transport in plant mitochondna in vivo.It is generally accepted that the free energy which is liberated from the redox reactions catalyzed by the respiratory chain is conserved as a proton electrochemical gradient across the inner mitochondrial membrane (2). The magnitude of this force has been shown in a number of systems to be unrelated to the rate of electron flux since the rate of respiration can be substantially inhibited by malonate or antimycin resulting in only a minor depression of the protonmotive force (6,8,21,24,27). This has been variously attributed to the nonohmic behavior of the inner membrane (5,15,27), to heterogeneity ofthe coupling of the mitochondria (11), to localized protonic coupling (29), and to variations in the stoichiometry of the redox driven proton pumps (redox slippage) (31). Estimates of the passive conductance of the inner membrane to protons in rat liver mitochondria (5,15) of respiration under ADP limited conditions (9) which has been attributed either to the activity of an endogenous H+/ K+ antiporter (8, 13) and/or to the operation of nonphosphorylative pathways (22). It has been suggested that nonphosphorylative pathways such as the alternative and rotenone-insensitive pathways constitute a natural slippage (or energy overflow) pathway in plant mitochondria (10, 16) (since they bypass the proton-pumping sites) and, as such, modulation of proton conductance may not be as important as in other tissues.In contrast to this suggestion there is some evidence in the literature to suggest that proton conductance does regulate respiratory activity. For instance, in isolated mitochondria it has been found that the state 4 rate is generally much slower than the rate of respiration prior to the initial addition of ADP (7) and, furthermore, that the decreased respiratory rate is associated with an increased membrane potential (7,22). These differences have been attributed to the build-up of endogenous ATP and decreased H+ conductance through the ATPase (7). However, the mechanism whereby this results in a decreased respirator...

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Pyruvate transport by thermogenic-tissue mitochondria

Cited by 23 publications

References 18 publications

Inhibition of Mitochondrial Pyruvate Transport by Zaprinast Causes Massive Accumulation of Aspartate at the Expense of Glutamate in the Retina

Inhibition of Mitochondrial Pyruvate Transport by Zaprinast Causes Massive Accumulation of Aspartate at the Expense of Glutamate in the Retina

Developmental Regulation of Respiratory Activity in Pea Leaves

Role of Nonohmicity in the Regulation of Electron Transport in Plant Mitochondria

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