Transplasma-membrane redox systems in growth and development

Crane, F.L.; Sun, I. L.; Clark, Michael G.; Grebing, C.; Löw, H.

doi:10.1016/0304-4173(85)90013-8

Cited by 442 publications

(175 citation statements)

References 208 publications

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“…in the presence of cytochalasin B) it degraded extracellularly to an unknown, single product that was not taken up by HepG2 cells and accounted for the apparent loss of stoichiometry in Figure 2(D). Although the above results suggest that DHA uptake was required for extracellular AH accumulation, the possibility nevertheless remained that cytochalasin B disrupted the transplasma membrane electron transport system [11] that might transduce extracellular reduction. The activity of transplasma membrane electron transport in HepG2 cells was therefore determined by the rate of ferricyanide reduction, as described previously [11].…”

Section: Resultsmentioning

confidence: 91%

“…Although the above results suggest that DHA uptake was required for extracellular AH accumulation, the possibility nevertheless remained that cytochalasin B disrupted the transplasma membrane electron transport system [11] that might transduce extracellular reduction. The activity of transplasma membrane electron transport in HepG2 cells was therefore determined by the rate of ferricyanide reduction, as described previously [11]. In contrast with its effects on DHA uptake, cytochalasin B had no effect on extracellular ferricyanide reduction by HepG2 cells (Table 2), as has been demonstrated for HL-60 cells [27] and erythrocytes [28].…”

Section: Resultsmentioning

confidence: 91%

“…Several studies [12,27,45] have suggested that AH and NADH act as intracellular electron donors for transplasma membrane electron transport systems [11] that transfer electrons to extracellular acceptors and hence might participate in the maintenance of extracellular AH. In addition, electrons might be transferred to plasma membrane monodehydroascorbate reductases, thereby maintaining extracellular AH under oxidative conditions that produce ascorbyl radicals [46].…”

Section: Discussionmentioning

confidence: 99%

“…A number of potential recycling mechanisms for extracellular AH have been described. These include the disproportionation [1] or extracellular reduction [10] of ascorbyl radicals via a transplasma membrane electron transport system [11], and the recycling of AH by human blood cells Abbreviations used : AH, ascorbate ; DHA, dehydroascorbic acid ; DIDS, 4,4h-di-isothiocyanostilbene-2,2h-disulphonate ; HBSS, Hanks balanced salt solution ; HUVEC, human umbilical-vein endothelial cells ; PBMC, peripheral blood mononuclear cells ; p-CMBS, p-chloromercuribenzylsulphonate ; PMN, polymorphonuclear leucocytes. 1 To whom correspondence should be addressed (e-mail biochemistry!hri.org.au).…”

Section: Introductionmentioning

confidence: 99%

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Efflux of hepatic ascorbate: a potential contributor to the maintenance of plasma vitamin C

Upston

Karjalainen

Bygrave

et al. 1999

Biochemical Journal

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Ascorbate (AH, the reduced form of vitamin C) is an important radical scavenger and antioxidant in human plasma; the resulting ascorbyl radical can disproportionate to AH and dehydroascorbic acid (DHA). Here we address potential maintenance mechanism(s) for extracellular AH by examining the ability of cells to convert extracellularly presented DHA to AH. DHA was rapidly transported into human liver (HepG2), endothelial and whole blood cells invitro by plasma membrane glucose transporters and reduced intracellularly. Liver cells displayed the highest capacity to release the intracellularly accumulated AH. The proteins responsible for DHA uptake and AH release could be distinguished by inhibitor studies. Thus, unlike DHA uptake, AH efflux was largely insensitive to cytochalasin B and thiol-reactive agents but was inhibited by phloretin, 4,4′-di-isothiocyanostilbene-2,2′-disulphonate and isoascorbate. Efflux of AH from cells was temperature-sensitive and saturable with a low affinity (millimolar, intracellular) for AH. In addition to isolated liver cells, perfusion of intact rat and guinea-pig liver with DHA resulted in AH in the circulating perfusate. Our results show that hepatocytes take up and reduce DHA and subsequently release part of the AH formed, probably via a membrane transporter. By converting extracellular DHA to extracellular AH, the liver might contribute to the maintenance of plasma AH, a process that could be important under conditions of oxidative stress.

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Section: Resultsmentioning

confidence: 91%

Section: Resultsmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Efflux of hepatic ascorbate: a potential contributor to the maintenance of plasma vitamin C

Upston

Karjalainen

Bygrave

et al. 1999

Biochemical Journal

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“…One such line of evidence is related to the description and characterization of a plasma membrane redox system apparently ubiquitously distributed throughout the animal and plant kingdom (for review see [39]). The system, termed ferricyanide reductase or NADH: ferricyanide oxidoreductase, has been shown to be able to reduce extracellular electron acceptors by furnishing reducing equivalents from cytosolic NADH to the cell surface.…”

Section: Thorstensen Unpublished Work)mentioning

confidence: 99%

The role of transferrin in the mechanism of cellular iron uptake

Thorstensen

Romslo

1990

Biochemical Journal

185

106

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INTRODUCTIONThe role of transferrin and its cell surface receptor in cellular iron metabolism has received considerable interest during the last decade. Hence, over this period several reviews covering various aspects of the topic have been published.In this review we attempt to summarize the new knowledge and controversies encountered during the last 4-5 years. The focus is on iron metabolism by the hepatocyte. We also view the concept of transferrin-cell interactions from angles which previously may not have been given particular attention, and we include some aspects of iron metabolism not normally covered by reviews of this type. Central parts of what may be regarded as well-established knowledge either have been entirely omitted, or are only briefly described or mentioned to the extent considered relevant to the particular topic discussed. Important aspects of iron metabolism such as iron adsorption, haemochromatosis, ferritin iron and iron in infection and neoplasia are not covered in the present paper. Instead, the reader is referred to one or more of the recently published reviews [1-5] and references therein.

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