Cell surface oxygen consumption: A major contributor to cellular oxygen consumption in glycolytic cancer cell lines

Herst, Patries M.; Berridge, Michael V.

doi:10.1016/j.bbabio.2006.11.018

Cited by 153 publications

(150 citation statements)

References 47 publications

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“…3B, left part), consistent with their cell metabolism existing in a state of aerobic glycolysis required to support continuous rapid proliferation. In contrast, the OCR of proliferation-arrested TRPM7-KO cells decreased to an absolute rate approaching what has previously been reported for quiescent primary thymocytes, 26,31 and essentially no change in OCR was observed upon glucose deprivation. These observations indicate that the proliferation-arrested TRPM7-deficient cells have transitioned to a metabolic state in which they have low energy needs, and those needs are met primarily through mitochondrial respiration.…”

Section: Trpm7-deficient Cells Maintained In Regular Mediamentioning

confidence: 42%

TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes

et al. 2010

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Section: Trpm7-deficient Cells Maintained In Regular Mediamentioning

confidence: 42%

TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes

et al. 2010

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“…NaN 3 inhibited consumption by 55%, indicating that a significant fraction of oxygen consumed was used for free radical production. DPI inhibited oxygen consumption by 70%, suggesting considerable oxidation of oxygen at the cell surface (34). Results in MNPCs were rather different; myxothiazol had minimal influence, inhibiting oxygen consumption by only 7%.…”

Section: Resultsmentioning

confidence: 91%

Notochordal intervertebral disc cells: Sensitivity to nutrient deprivation

Guehring

Wilde

Sumner

et al. 2009

Arthritis & Rheumatism

119

164

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Objective. The nucleus pulposus (NP) of the intervertebral disc develops from the notochord. Humans and other species in which notochordal cells (NCs) disappear to be replaced by chondrocyte-like mature NP cells (MNPCs) frequently develop disc degeneration, unlike other species that retain NCs. The reasons for NC disappearance are unknown. In humans, the change in cell phenotype (to MNPCs) coincides with changes that decrease nutrient supply to the avascular disc. We undertook this study to test the hypothesis that the consequent nutrient stress could be associated with NC disappearance.Methods. We measured cell densities and metabolic rates in 3-dimensional cultures of porcine NCs and bovine MNPCs, and we determined survival rates under conditions of nutrient deprivation. We used scanning electron microscopy to examine end plate porosity of discs with NCs and those with MNPCs. Nutrientmetabolite profiles and cell viability were calculated as a function of cell density and disc size in a consumption/ diffusion mathematical model.Results. NCs were more active metabolically and more susceptible to nutrient deprivation than were MNPCs. Hypoxia increased rates of glycolysis in NCs but not in MNPCs. Higher end plate porosity in discs with NCs suggested greater nutrient supply in keeping with higher nutritional demands. Mathematical simulations and experiments using an analog disc diffusion chamber indicated that a fall in nutrient concentrations resulting from increased diffusion distance during growth and/or a fall in blood supply through end plate changes could instigate NC disappearance.Conclusion. NCs demand more energy and are less resistant to nutritional stress than MNPCs, which may shed light on the fate of NCs in humans. This provides important information about prospective NC tissue engineering approaches.The intervertebral discs are cartilaginous structures interspersed between the vertebral bodies, providing flexibility to the spinal column. They consist of 3 regions: the outer annulus fibrosus (AF) surrounding the inner nucleus pulposus (NP) and a thin hyaline cartilaginous end plate lying between the disc and the adjacent vertebral bodies. The AF and NP differ in developmental origin, with the annulus arising from the mesenchyme and the nucleus from the notochord (1,2). During development the highly hydrated NP is populated by clusters of large vacuolated notochordal cells (NCs) of distinct molecular phenotype (2,3). In humans and some other species (e.g., cattle, chondrodystrophoid dogs) but not in others (e.g., rodents, pigs), NCs disappear before maturity to be replaced by chondrocyte-like cells of unknown provenance (here called mature NP cells [MNPCs]), which synthesize a more collagenous and less hydrated matrix (1,4-6).

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“…The second is that the amount of O 2 being consumed by oxidases and oxygenases other than cytochrome c oxidase has increased. Nonmitochondrial VO 2 has been described (Figure 11)57, 58 and these reactions do not involve nicotinamide adenine dinucleotide or FADH 2 in mitochondria, and therefore are not coupled to CO 2 created by the Krebs cycle. Enzymes such as nicotinamide adenine dinucleotide phosphate oxidases, cytochrome p450 oxidases, monoamine oxidases, and xanthine oxidases59 primarily oxidize water without a concomitant production of CO 2 .…”

Section: Discussionmentioning

confidence: 99%

Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post–Cardiac Arrest Rat: A Novel Metabolic Phenotype

Shinozaki

Becker

Saeki³

et al. 2018

JAHA

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BackgroundThe concept that resuscitation from cardiac arrest (CA) results in a metabolic injury is broadly accepted, yet patients never receive this diagnosis. We sought to find evidence of metabolic injuries after CA by measuring O2 consumption and CO2 production (VCO 2) in a rodent model. In addition, we tested the effect of inspired 100% O2 on the metabolism.Methods and ResultsRats were anesthetized and randomized into 3 groups: resuscitation from 10‐minute asphyxia with inhaled 100% O2 (CA–fraction of inspired O2 [FIO2] 1.0), with 30% O2 (CA‐FIO 2 0.3), and sham with 30% O2 (sham‐FIO 2 0.3). Animals were resuscitated with manual cardiopulmonary resuscitation. The volume of extracted O2 (VO 2) and VCO 2 were measured for a 2‐hour period after resuscitation. The respiratory quotient (RQ) was RQ=VCO 2/VO 2. VCO 2 was elevated in CA‐FIO 2 1.0 and CA‐FIO 2 0.3 when compared with sham‐FIO 2 0.3 in minutes 5 to 40 after resuscitation (CA‐FIO 2 1.0: 16.7±2.2, P<0.01; CA‐FIO 2 0.3: 17.4±1.4, P<0.01; versus sham‐FIO 2 0.3: 13.6±1.1 mL/kg per minute), and then returned to normal. VO 2 in CA‐FIO 2 1.0 and CA‐FIO 2 0.3 increased gradually and was significantly higher than sham‐FIO 2 0.3 2 hours after resuscitation (CA‐FIO 2 1.0: 28.7±6.7, P<0.01; CA‐FIO 2 0.3: 24.4±2.3, P<0.01; versus sham‐FIO 2 0.3: 15.8±2.4 mL/kg per minute). The RQ of CA animals persistently decreased (CA‐FIO 2 1.0: 0.54±0.12 versus CA‐FIO 2 0.3: 0.68±0.05 versus sham‐FIO 2 0.3: 0.93±0.11, P<0.01 overall).Conclusions CA altered cellular metabolism resulting in increased VO 2 with normal VCO 2. Normal VCO 2 suggests that the postresuscitation Krebs cycle is operating at a presumably healthy rate. Increased VO 2 in the face of normal VCO 2 suggests a significant alteration in O2 utilization in postresuscitation. Several RQ values fell well outside the normally cited range of 0.7 to 1.0. Higher FIO 2 may increase VO 2, leading to even lower RQ values.

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Cell surface oxygen consumption: A major contributor to cellular oxygen consumption in glycolytic cancer cell lines

Cited by 153 publications

References 47 publications

TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes

TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes

Notochordal intervertebral disc cells: Sensitivity to nutrient deprivation

Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post–Cardiac Arrest Rat: A Novel Metabolic Phenotype

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