Coenzyme Q reductase from liver plasma membrane: purification and role in trans-plasma-membrane electron transport.

Villalba, José M.; Navarro, Francisco; Córdoba, Francisco; Serrano, Antonio; Arroyo, Antonio; Crane, F.L.; Navas, Plácido

doi:10.1073/pnas.92.11.4887

Cited by 158 publications

(100 citation statements)

References 12 publications

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“…The addition of either ferricyanide or exogenous Q to growth media can replace the requirement of °cells for pyruvate (43)(44)(45). The exogenous Q is known to function in a trans-plasma membrane electron transport system, where intracellular NADH is oxidized and electrons are transferred across the plasma membrane to a wide variety of extracellular acceptors, including ferricyanide (46,47). In fact, this trans-plasma membrane electron transport system is up-regulated in °cells (43), and there is a concomitant increase in the level of Q at the plasma membrane (48).…”

Section: Discussionmentioning

confidence: 99%

A dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants

Jonassen

Larsen

Clarke

2001

Proc. Natl. Acad. Sci. U.S.A.

165

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Mutations in the clk-1 gene of the nematode Caenorhabditis elegans result in slowed development, sluggish adult behaviors, and an increased lifespan. CLK-1 is a mitochondrial polypeptide with sequence and functional conservation from human to yeast. Coq7p, the Saccharomyces cerevisiae homologue, is essential for ubiquinone (coenzyme Q or Q) synthesis and therefore respiration. However, based on assays of respiratory function, it has been reported that the primary defect in the C. elegans clk-1 mutants is not in Q biosynthesis. How do the clk-1 mutant worms have essentially normal rates of respiration, when biochemical studies in yeast suggest a Q deficiency? Nematodes are routinely fed Escherichia coli strains containing a rich supply of Q. To study the Q synthesized by C. elegans, we cultured worms on an E. coli mutant that lacks Q and found that clk-1 mutants display early developmental arrest from eggs, or sterility emerging from dauer stage. Provision of Q-replete E. coli rescues these defects. Lipid analysis showed that clk-1 worms lack the nematode Q9 isoform and instead contain a large amount of a metabolite that is slightly more polar than Q9. The clk-1 mutants also have increased levels of Q8, the E. coli isoform, and rhodoquinone-9. These results show that the clk-1 mutations result in Q auxotrophy evident only when Q is removed from the diet, and that the aging and developmental phenotypes previously described are consistent with altered Q levels and distribution.

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Section: Discussionmentioning

confidence: 99%

A dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants

Jonassen

Larsen

Clarke

2001

Proc. Natl. Acad. Sci. U.S.A.

165

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“…In previous investigations, DCIP and FeCN have been used interchangeably (Larm et al 1994;Zurbriggen and Dreyer 1994;Vaillant et al 1996), and studies that showed FeCN reduction is ubiquinone-dependent did not measure DCIP reduction (Sun et al 1992;Villalba et al 1995). Biochemical analyses of purified plasma membranes have identified multiple PMOR activities in a homogeneous neuroblastoma cell line (Zurbriggen and Dreyer 1994).…”

Section: Discussionmentioning

confidence: 99%

CNS neurons express two distinct plasma membrane electron transport systems implicated in neuronal viability

Wright

Kühn

2002

Journal of Neurochemistry

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Trans-plasma membrane electron transport is critical for maintaining cellular redox balance and viability, yet few, if any, investigations have studied it in intact primary neurons. In this investigation, extracellular reduction of 2,6-dichloroindophenol (DCIP) and ferricyanide (FeCN) were measured as indicators of trans-plasma membrane electron transport by chick forebrain neurons. Neurons readily reduced DCIP, but not FeCN unless CoQ 1 , an exogenous ubiquinone analog, was added to the assays. CoQ 1 stimulated FeCN reduction in a dosedependent manner but had no effect on DCIP reduction. Reduction of both substrates was totally inhibited by e-maleimidocaproic acid (MCA), a membrane-impermeant thiol reagent, and slightly inhibited by superoxide dismutase. Diphenylene iodonium, a flavoenzyme inhibitor, completely inhibited FeCN reduction but had no affect on DCIP reduction, suggesting that these substrates are reduced by distinct redox pathways. The relationship between plasma membrane electron transport and neuronal viability was tested using the inhibitors MCA and capsaicin. MCA caused a dose-dependent decline in neuronal viability that closely paralleled its inhibition of both reductase activities. Similarly capsaicin, a NADH oxidase inhibitor, induced a rapid decline in neuronal viability. These results suggest that trans-plasma membrane electron transport helps maintain a stable redox environment required for neuronal viability.

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“…As a whole, both CoQ and its reductases ( Figure 1) constitute a transplasma membrane antioxidant redox system responsible of the above described functions. [51][52][53] The aforementioned antioxidants are maintained in their reduced forms at the plasma membrane by different CoQdependent reductases, NADH-dependent cytochrome b 5 reductase 53 and NAD(P)H:quinone-oxidoreductase-1 (NQO1). 55 Different dietary modifications can modulate these enzyme activities to protect the plasma membrane.…”

Section: Cr Increases Coenzyme Q-dependent Reductases In Plasma Membrmentioning

confidence: 99%

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Ungvári

Parrado-Fernández

Csiszár

et al. 2008

Circulation Research

218

189

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Abstract-This review focuses on the emerging evidence that attenuation of the production of reactive oxygen species and inhibition of inflammatory pathways play a central role in the antiaging cardiovascular effects of caloric restriction. Particular emphasis is placed on the potential role of the plasma membrane redox system in caloric restriction-induced pathways responsible for sensing oxidative stress and increasing cellular oxidative stress resistance. We propose that caloric restriction increases bioavailability of NO, decreases vascular reactive oxygen species generation, activates the Nrf2/antioxidant response element pathway, inducing reactive oxygen species detoxification systems, exerts antiinflammatory effects, and, thereby, suppresses initiation/progression of vascular disease that accompany aging. (Circ Res. 2008;102:519-528.)

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Coenzyme Q reductase from liver plasma membrane: purification and role in trans-plasma-membrane electron transport.

Cited by 158 publications

References 12 publications

A dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants

A dietary source of coenzyme Q is essential for growth of long-lived Caenorhabditis elegans clk-1 mutants

CNS neurons express two distinct plasma membrane electron transport systems implicated in neuronal viability

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

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