The effects of lipid fluidity on the rotational diffusion of complex I and complex III in reconstituted NADH-cytochrome c oxidoreductase

Poore, Veronica M.; Fitzsimons, J.T.R; Ragan, C I

doi:10.1016/0005-2736(82)90477-1

Cited by 14 publications

(14 citation statements)

References 33 publications

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“…Abnormalities in lipid order of the inner mitochondrial membrane may reduce linked I/III activity without altering I or III activity individually by a number of mechanisms, such as impaired association of complex I and III into a supercomplex, restricted ubiquinone movement within the membrane, and decreased accessibility of ubiquinone to its site of reduction in complex I (29,42,54,55). Lenaz and coworkers (as reviewed in reference 37) have suggested that the concentration of ubiquinone available locally to complexes I and/or III in the membrane, and not ubiquinone movement between complex I and III per se, is rate limiting in complex I/III activity.…”

Section: Cardiolipin Biosynthesis the Brains Of Sncamentioning

confidence: 99%

Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein

Ellis

Murphy

Mitchell

et al. 2005

Molecular and Cellular Biology

252

210

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The presynaptic protein ␣-synuclein, implicated in Parkinson disease (PD), binds phospholipids and has a role in brain fatty acid (FA) metabolism. In mice lacking ␣-synuclein (Snca ؊/؊ ), total brain steady-state mass of the mitochondria-specific phospholipid, cardiolipin, is reduced 22% and its acyl side chains show a 51% increase in saturated FAs and a 25% reduction in essential n-6, but not n-3, polyunsaturated FAs. Additionally, 23% reduction in phosphatidylglycerol content, the immediate biosynthetic precursor of cardiolipin, was observed without alterations in the content of other brain phospholipids. Consistent with these changes, more ordered lipid head group and acyl chain packing with enhanced rotational motion of diphenylhexatriene (DPH) about its long axis were demonstrated in time-resolved DPH fluorescence lifetime experiments. These abnormalities in mitochondrial membrane properties were associated with a 15% reduction in linked complex I/III activity of the electron transport chain, without reductions in mitochondrial number, complex II/III activity, or individual complex I, II, III, or IV activity. Reduced complex I activity is thought to be a critical factor in the development of PD. Thus, altered membrane composition and structure and impaired complex I/III function in Snca ؊/؊ brain suggest a relationship between ␣-synuclein's role in brain lipid metabolism, mitochondrial function, and PD.

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Section: Cardiolipin Biosynthesis the Brains Of Sncamentioning

confidence: 99%

Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein

Ellis

Murphy

Mitchell

et al. 2005

Molecular and Cellular Biology

252

210

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“…The advantages of using a reconstituted system were, firstly, that the ratio of Complex III to Complex I could be manipulated so as to give an initial high level of quinone reduction and, secondly, that the cytochrome c concentration could be more readily controlled. In several previous papers [16][17][18][19] we have described the properties of the reconstituted NADH: cytochrome c reductase. In the presence of ubiquinone and low concentrations of exogenous phospholipid, the interaction between Complex I and Complex III behaves exactly as expected for first-order kinetics of quinone oxidoreduction, as shown, for example, by the dependence of velocity on the molar ratio of the two Complexes [16].…”

Section: Resultsmentioning

confidence: 99%

“…The reconstituted membranes do not present a permeability barrier to either NADH or cytochrome c, and the kinetic properties of the system are consistent with all molecules of the complexes having access to a single quinone pool. The reconstituted system consists apparently of vesicular membranes (despite the absence ofa permeability -barrier) in which the prontein molecules are randomly distributed and in rapid motion [19].…”

Section: Resultsmentioning

confidence: 99%

The effect of rate limitation by cytochrome c on the redox state of the ubiquinone pool in reconstituted NADH: cytochrome c reductase

Reed

Ragan

1987

Biochemical Journal

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The kinetic model of Ragan & Cottingham [(1985) Biochim. Biophys. Acta 811, 13-31] for electron transport through a mobile pool of quinone predicts that, under certain conditions, the normal linear dependence of electron flow on the degree of reduction (or oxidation) of the quinone should no longer be found. These conditions can be met by reconstituted NADH: cytochrome c reductase (Complex I-III from bovine heart) when electron flow is rate-limited by a low concentration of cytochrome c. We show that, in such a system, the dependence of activity (varied by inhibition with rotenone) on the steady-state level of quinone reduction is indeed non-linear and very closely accounted for by the theory.

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“…In the absence of such fluidity, electron flow in mitochondria from hibernating animals might be confined to the -2O-30% of bcr molecules which form direct complexes with the dehydrogenases [14] without involvement of the CoQ pool.…”

Section: Discussionmentioning

confidence: 99%

Reversible inhibition of electron transfer in the ubiquinol

et al. 1990

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Electron transfer through the ubiquinol:cytochrome c 1‐segment of liver mitochondria isolated from hibernating ground squirrels Citellus undulatus is repressed by 70–80% as compared to mitochondria from the active animals. The inhibition site is likely to be localized between ubiquinone and the cytochrome bc 1, complex. Partial release of the inhibition can be observed upon swelling of the isolated mitochondria in a hypoosmotie medium, the effect being prevented by phospholipase A2 inhibitors. Possible role of phospholipase A2 in regulation of ubiquinol oxidation by complex bc 1, is discussed.

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The effects of lipid fluidity on the rotational diffusion of complex I and complex III in reconstituted NADH-cytochrome c oxidoreductase

Cited by 14 publications

References 33 publications

Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein

Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein

The effect of rate limitation by cytochrome c on the redox state of the ubiquinone pool in reconstituted NADH: cytochrome c reductase

Reversible inhibition of electron transfer in the ubiquinol

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