Relevant bibliographies by topics / Cellular bioenergetics

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Cellular bioenergetics'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cellular bioenergetics"

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Hill, Bradford G., Gloria A. Benavides, Jack R. Lancaster, Scott Ballinger, Lou Dell’Italia, Jianhua Zhang, and Victor M. Darley-Usmar. "Integration of cellular bioenergetics with mitochondrial quality control and autophagy." Biological Chemistry 393, no. 12 (December 1, 2012): 1485–512. http://dx.doi.org/10.1515/hsz-2012-0198.

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Abstract Bioenergetic dysfunction is emerging as a cornerstone for establishing a framework for understanding the pathophysiology of cardiovascular disease, diabetes, cancer and neurodegeneration. Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.
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Augsburger, Fiona, Elisa B. Randi, Mathieu Jendly, Kelly Ascencao, Nahzli Dilek, and Csaba Szabo. "Role of 3-Mercaptopyruvate Sulfurtransferase in the Regulation of Proliferation, Migration, and Bioenergetics in Murine Colon Cancer Cells." Biomolecules 10, no. 3 (March 13, 2020): 447. http://dx.doi.org/10.3390/biom10030447.

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3-mercaptopyruvate sulfurtransferase (3-MST) has emerged as one of the significant sources of biologically active sulfur species in various mammalian cells. The current study was designed to investigate the functional role of 3-MST’s catalytic activity in the murine colon cancer cell line CT26. The novel pharmacological 3-MST inhibitor HMPSNE was used to assess cancer cell proliferation, migration and bioenergetics in vitro. Methods included measurements of cell viability (MTT and LDH assays), cell proliferation and in vitro wound healing (IncuCyte) and cellular bioenergetics (Seahorse extracellular flux analysis). 3-MST expression was detected by Western blotting; H2S production was measured by the fluorescent dye AzMC. The results show that CT26 cells express 3-MST protein and mRNA, as well as several enzymes involved in H2S degradation (TST, ETHE1). Pharmacological inhibition of 3-MST concentration-dependently suppressed H2S production and, at 100 and 300 µM, attenuated CT26 proliferation and migration. HMPSNE exerted a bell-shaped effect on several cellular bioenergetic parameters related to oxidative phosphorylation, while other bioenergetic parameters were either unaffected or inhibited at the highest concentration of the inhibitor tested (300 µM). In contrast to 3-MST, the expression of CBS (another H2S producing enzyme which has been previously implicated in the regulation of various biological parameters in other tumor cells) was not detectable in CT26 cells and pharmacological inhibition of CBS exerted no significant effects on CT26 proliferation or bioenergetics. In summary, 3-MST catalytic activity significantly contributes to the regulation of cellular proliferation, migration and bioenergetics in CT26 murine colon cancer cells. The current studies identify 3-MST as the principal source of biologically active H2S in this cell line.
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Lehrer, H. Matthew, Lauren Chu, Martica Hall, and Kyle Murdock. "009 Self-Reported Sleep Efficiency and Duration are Associated with Systemic Bioenergetic Function in Community-Dwelling Adults." Sleep 44, Supplement_2 (May 1, 2021): A4. http://dx.doi.org/10.1093/sleep/zsab072.008.

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Abstract Introduction Sleep is important for aging, health, and disease, but its cellular role in these outcomes is poorly understood. Basic research suggests that disturbed and insufficient sleep impair mitochondrial bioenergetics, which is involved in numerous aging-related chronic conditions. However, the relationship between sleep and bioenergetics has not been examined in humans. We examined associations of self-reported sleep with systemic bioenergetic function in peripheral blood mononuclear cells (PBMCs) of community-dwelling adults. Methods N = 43 adults (79% female) ages 48–70 (M = 61.63, SD = 5.99) completed the Pittsburgh Sleep Quality Index (PSQI) from which key components of sleep (satisfaction, alertness, timing, efficiency, and duration) were calculated. Participants provided blood samples from which PBMCs were isolated and measured for bioenergetics using extracellular flux analysis. Associations of sleep components with bioenergetic parameters, including the Bioenergetic Health Index (BHI), were examined. Results In bivariate analyses, lower sleep efficiency was associated with lower maximal respiration, spare capacity, and BHI (ps < 0.05). Longer sleep duration was associated with lower BHI (p < 0.01) and later sleep timing was associated with higher basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and non-mitochondrial respiration (ps < 0.05). After adjustment for age, sex, and body mass index, lower sleep efficiency (β = 0.52, p < 0.01) and longer sleep duration (β = -0.43, p < 0.01) were associated with lower BHI. Conclusion Self-reported indices of sleep efficiency and duration are related to systemic bioenergetic function in humans, suggesting a possible cellular pathway linking sleep to health. Support (if any) T32HL082610
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Welch, G. R. "Bioenergetics and the cellular microenvironment." Pure and Applied Chemistry 65, no. 9 (January 1, 1993): 1907–14. http://dx.doi.org/10.1351/pac199365091907.

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Acuña-Castroviejo, Darío, Miguel Martín, Manuel Macías, Germaine Escames, Josefa León, Huda Khaldy, and Russel J. Reiter. "Melatonin, mitochondria, and cellular bioenergetics." Journal of Pineal Research 30, no. 2 (March 2001): 65–74. http://dx.doi.org/10.1034/j.1600-079x.2001.300201.x.

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Heiden, Matthew Vander. "Cellular Bioenergetics in Lymphoid Neoplasia." Blood 118, no. 21 (November 18, 2011): SCI—25—SCI—25. http://dx.doi.org/10.1182/blood.v118.21.sci-25.sci-25.

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Abstract Abstract SCI-25 Many cancer cells metabolize glucose by aerobic glycolysis, a phenomenon characterized by increased glycolysis with lactate production and decreased oxidative phosphorylation. We have argued that alterations in cell metabolism associated with cancer may be selected by cancer cells to meet the distinct metabolic needs of proliferation. Unlike metabolism in differentiated cells, which is geared toward efficient ATP generation, the metabolism in cancer cells must be adapted to facilitate the accumulation of biomass. Cancer cells divert a larger fraction of their nutrient metabolism to pathways other than mitochondrial respiration regardless of oxygen availability. Nevertheless, oxygen levels still influence how nutrients are metabolized. We have found that the source of carbon used in various anabolic processes varies based on oxygen levels. Furthermore, the enzymes used to metabolize nutrients can also differ based on the cellular context. This includes regulation of isocitrate dehydrogenase, an enzyme that is mutated in some cancers. There is also strong selection for use of the M2 isoform of pyruvate kinase (PK-M2) to metabolize glucose in cancer cell lines. However, evidence from mouse models suggests that PK-M2 is dispensable for glucose metabolism by many tumors in vivo, suggesting an alternate pathway to convert phosphoenolpyruvate to pyruvate can be used to metabolize glucose. This regulation of pyruvate kinase also plays an important role in hematopoietic stem cell biology. Together, these findings argue that distinct metabolic phenotypes exist among proliferating cells, and both environmental and genetic factors influence how metabolism is regulated to support cell growth. Disclosures: Vander Heiden: Agios Pharmaceuticals: Consultancy, Equity Ownership.
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Davies, Karen M., and Bertram Daum. "Role of cryo-ET in membrane bioenergetics research." Biochemical Society Transactions 41, no. 5 (September 23, 2013): 1227–34. http://dx.doi.org/10.1042/bst20130029.

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To truly understand bioenergetic processes such as ATP synthesis, membrane-bound substrate transport or flagellar rotation, systems need to be analysed in a cellular context. Cryo-ET (cryo-electron tomography) is an essential part of this process, as it is currently the only technique which can directly determine the spatial organization of proteins at the level of both the cell and the individual protein complexes. The need to assess bioenergetic processes at a cellular level is becoming more and more apparent with the increasing interest in mitochondrial diseases. In recent years, cryo-ET has contributed significantly to our understanding of the molecular organization of mitochondria and chloroplasts. The present mini-review first describes the technique of cryo-ET and then discusses its role in membrane bioenergetics specifically in chloroplasts and mitochondrial research.
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Chacko, Balu K., Philip A. Kramer, Saranya Ravi, Gloria A. Benavides, Tanecia Mitchell, Brian P. Dranka, David Ferrick, et al. "The Bioenergetic Health Index: a new concept in mitochondrial translational research." Clinical Science 127, no. 6 (May 29, 2014): 367–73. http://dx.doi.org/10.1042/cs20140101.

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Bioenergetics has become central to our understanding of pathological mechanisms, the development of new therapeutic strategies and as a biomarker for disease progression in neurodegeneration, diabetes, cancer and cardiovascular disease. A key concept is that the mitochondrion can act as the ‘canary in the coal mine’ by serving as an early warning of bioenergetic crisis in patient populations. We propose that new clinical tests to monitor changes in bioenergetics in patient populations are needed to take advantage of the early and sensitive ability of bioenergetics to determine severity and progression in complex and multifactorial diseases. With the recent development of high-throughput assays to measure cellular energetic function in the small number of cells that can be isolated from human blood these clinical tests are now feasible. We have shown that the sequential addition of well-characterized inhibitors of oxidative phosphorylation allows a bioenergetic profile to be measured in cells isolated from normal or pathological samples. From these data we propose that a single value–the Bioenergetic Health Index (BHI)–can be calculated to represent the patient's composite mitochondrial profile for a selected cell type. In the present Hypothesis paper, we discuss how BHI could serve as a dynamic index of bioenergetic health and how it can be measured in platelets and leucocytes. We propose that, ultimately, BHI has the potential to be a new biomarker for assessing patient health with both prognostic and diagnostic value.
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Narchi, Hassib, Pramathan Thachillath, and Abdul-Kader Souid. "Forebrain cellular bioenergetics in neonatal mice." Journal of Neonatal-Perinatal Medicine 11, no. 1 (April 16, 2018): 79–86. http://dx.doi.org/10.3233/npm-181737.

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Acin-Perez, Rebeca, Cristiane Benincá, Byourak Shabane, Orian S. Shirihai, and Linsey Stiles. "Utilization of Human Samples for Assessment of Mitochondrial Bioenergetics: Gold Standards, Limitations, and Future Perspectives." Life 11, no. 9 (September 10, 2021): 949. http://dx.doi.org/10.3390/life11090949.

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Mitochondrial bioenergetic function is a central component of cellular metabolism in health and disease. Mitochondrial oxidative phosphorylation is critical for maintaining energetic homeostasis, and impairment of mitochondrial function underlies the development and progression of metabolic diseases and aging. However, measurement of mitochondrial bioenergetic function can be challenging in human samples due to limitations in the size of the collected sample. Furthermore, the collection of samples from human cohorts is often spread over multiple days and locations, which makes immediate sample processing and bioenergetics analysis challenging. Therefore, sample selection and choice of tests should be carefully considered. Basic research, clinical trials, and mitochondrial disease diagnosis rely primarily on skeletal muscle samples. However, obtaining skeletal muscle biopsies requires an appropriate clinical setting and specialized personnel, making skeletal muscle a less suitable tissue for certain research studies. Circulating white blood cells and platelets offer a promising primary tissue alternative to biopsies for the study of mitochondrial bioenergetics. Recent advances in frozen respirometry protocols combined with the utilization of minimally invasive and non-invasive samples may provide promise for future mitochondrial research studies in humans. Here we review the human samples commonly used for the measurement of mitochondrial bioenergetics with a focus on the advantages and limitations of each sample.
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Dissertations / Theses on the topic "Cellular bioenergetics"

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Spickett, Corinne Michelle. "NMR studies of cellular bioenergetics." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257961.

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Cui, Xiaoyu. "Regulation of Cellular Bioenergetics by Na/K-ATPase." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1481294995657855.

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Kelly, R. A. "Biochemical thermodynamic modelling of cellular bioenergetics : a quantitative systems pharmacology approach." Thesis, Liverpool John Moores University, 2018. http://researchonline.ljmu.ac.uk/7754/.

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In this thesis, thermodynamic-based mathematical modelling is combined with experimental in vitro extracellular flux analysis in order to assess drug redox cycling and cellular bioenergetics. It is widely accepted that pharmacological activity of certain classes of drugs (e.g. anticancer, antimalarial) is related to their ability to accept one or two electrons. However, pharmacological activity via redox cycling is an understated mechanism of toxicity associated with many classes of drugs. In particular, oxidative stress as a result of redox cycling plays a pivotal role in the cause of cardiac toxicity. For example, doxorubicin is an anti-neoplastic drug used to treat cancer. It has strong links to redox cycling-induced cardiac toxicity associated directly with elevated levels of reactive oxygen species (ROS) and oxidative stress within the mitochondria. The underlying mechanisms of redox cycling is very difficult to elucidate, due to the fleeting existence of the radical species. However, assessment of such cellular bioenergetics can be ameliorated with the aid of computational assistance. In chapter 2 the development of a novel thermodynamic-based in silico model of doxorubicin redox cycling is described, which is parameterized using data from in vitro extracellular flux analysis. The model is used to simulate mitochondrial-specific ROS, with its outputs confirmed against in vitro data. Chapter 3 describes construction of a pH-dependent thermodynamic model of hepatic glycolytic flux, used to determine the role of the monocarboxylate transporter 1 flux during extracellular acidification. Finally, chapter 4 describes a thermodynamic-based in silico model of mitochondrial bioenergetics, capable of simulating oxygen consumption rates of a cohort of in vitro human primary hepatocyte data. The model is finally used to simulate perturbations in key bioenergetic variables and reaction fluxes, illustrating the resulting changes on mitochondrial pH, membrane potential and subsequent oxygen consumption rates.
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Štajer, Valdemar. "EFEKTI AEROBNOG I ANAEROBNOG VEŽBANjA MAKSIMALNOG INTENZITETA NA BIOMARKERE PERIFERNOG ZAMORA I ĆELIJSKE BIOENERGETIKE KOD MLADIH MUŠKARACA I ŽENA." Phd thesis, Univerzitet u Novom Sadu, Fakultet sporta i fizičkog vaspitanja u Novom Sadu, 2019. https://www.cris.uns.ac.rs/record.jsf?recordId=111943&source=NDLTD&language=en.

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Primena biomarkera ćelijske energetike, uključujući indikatore metabolizma kreatina u krvi, je relativno novijeg datuma, gde se ovi indikatori koriste kao mogući pokazatelji stanja organizma pri maksimalno intenzivnim fizičkim aktivnostima. Cilj istraživanja je obuhvatao utvrđivanje efekata pojedinačnih epizoda aerobnog i anaerobnog vežbanja maksimalnog intenziteta na biomarkere perifernog zamora i ćelijske bioenergetike kod mladih muškaraca i žena. Istraživanje je dizajnirano tako da obuhvati populaciju fizički aktivnih muškaraca i žena, kao i populaciju aktivnih sportista. U prvom eksperimentalnom tretmanu fizički aktivni ispitanici muškog (n =12) i ženskog pola (n = 11) podvrgnuti su test protokolima aerobnog i anaerobnog opterećenja maksimalnog intenzivnog i kratkog trajanja. Tokom aerobnog test protokola ispitanici su trčali do maksimalnog voljnog otkaza na tredmil traci sa progresivnim povećanjem opterećenja. Pri anaerobnom test protokolu ispitanici su izvršili testiranje snažne izdržljivosti gornjih ekstremiteta do otkaza potiskom sa ravne klupe, uz opterećenje od 25% od njihove telesne težine. Drugi eksperimentalni tretman je sačinjen iz pre-eksperimentalnog testiranja kardiorespiratorne forme i eksperimentalne protokol sesije trčanja do maksimalnog voljnog otkaza na pokretnoj traci, pri konstantnoj individualnoj brzina trčanja na anaerobnom pragu. U ovom eksperimentalnom tretmanu bila je uključena populacija aktivnih sportista     (n = 10). Pre, tokom i nakon eksperimentalnih sesija praćena je koncentracija različitih biohemijskih i hematoloških markera: guanidinosirćetna kiselina (GAA); kreatin (Cr); kreatinin (Crn); laktat (Lac); interleukin-6 (IL-6); kreatin kinaza (CK); kortizol (Cor). Rezultati prvog eksperimentalnog tretmana su utvrdili statistički značajne promene u koncentraciji GAA, Cr i Crn u ktvi pre i nakon pojedinačne epizode aerobnog i anaerobnog vežbanja maksimalnim intenzitetom. Utvrđena je i statistički značajna povezanost između vežbanjem-indukovanih promena u cirkulatornim vrednostima GAA, Cr, Crn za vreme pre, tokom i nakon drugog eksperimentalnog tretmana. Uočena je statistički značajna povezanost između promena koncentracije GAA, Cr, Crn u serumu sa tradicionalnim biomarkerima perifernog zamora (IL6, Cor, Lac, CK). Dobijeni rezultati ukazuju na mogućnost primene biomarkera metabolizma kreatina u krvi prilikom praćenja i evaluacije stanja organizma tokom maksimalnih intenzivnih fizičkih aktivnosti kod mladih muškaraca i žena.
The use of biomarkers of cellular bioenergetics in exercise science appears more prevalent in recent years, where these outcomes perhaps describe changes in creatine metabolism during strenuous exercise. The aim of this study was to determine the effects of individual episodes of strenuous aerobic and anaerobic exercise on several biomarkers of peripheral fatigue and cellular bioenergetics in young men and women. The study recruited physically active men and women, and active athletes. In the first experiment, physically active men (n = 12) and women (n = 11) were subjected to strenuous aerobic and anaerobic exercise. During the aerobic test, subjects ran to exhaustion while during the anaerobic test, subjects performed repetitive bench press exercise. The second experimental treatment consisted of a pre-experimental testing of cardiorespiratory fitness, and an experimental protocol of a strenuous running session to exhaustion at constant individual running speed at the anaerobic threshold; active athletes (n = 10) were included in this experimental treatment. The blood levels of various biochemical and hematological markers were monitored before, during and after the experimental sessions, including guanidinoacetic acid (GAA); creatine (Cr); creatinine (Crn); lactate (Lac); interleukin-6 (IL-6); creatine kinase (CK); cortisol (Cor), and plethora of other physiological outcomes. We found statistically significant changes in serum GAA, Cr and Crn before and after a single session of strenuous aerobic and anaerobic exercise. A significant correlation was found between exercise-induced changes in serum GAA, Cr and Crn before, during and after the second experimental intervention. A statistically significant association was observed between changes in serum GAA, Cr, Crn and traditional biomarkers of peripheral fatigue (IL6, Cor, Lac, CK). The results of the present study suggest that biomarkers of creatine metabolism might be used as innovative tools in monitoring strenuous exercise in young men and women.
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Buranasudja, Visarut. "DNA damage and disruption of cellular bioenergetics contribute to the anti-cancer effects of pharmacological ascorbate." Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6551.

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The clinical potential of pharmacological ascorbate (P-AscH-; IV delivery achieving mM concentrations in blood) as an adjuvant in cancer therapy is being re-evaluated. At mM concentrations, P-AscH- is thought to exhibit anti-cancer activity via generation of a flux of H2O2 in tumors, which leads to oxidative distress. Here, we use cell culture models of pancreatic cancer, MIA PaCa-2, PANC-1, and 339 cells, to examine the effects of P-AscH- on DNA damage, and downstream consequences, including changes in bioenergetics. We have found that the high flux of H2O2 produced by P-AscH- induces both nuclear and mitochondrial DNA damage. In response to this DNA damage, we observed that poly (ADP-ribose) polymerase-1 (PARP-1) is hyperactivated, as determined by increased formation of poly (ADP-ribose) polymer. Using our unique absolute quantitation, we found that the P-AscH--mediated the overactivation of PARP-1, which results in consumption of NAD+, and subsequently depletion of ATP (potential energy crisis) leading to mitotic cell death. Time-course studies with MIA PaCa-2 cells showed that the level of NAD+ and ATP were reduced by 80% immediately after a 1-h exposure to P-AscH- (4 mM; 14 pmol cell-1); both species returned to near basal levels within 24 h. In parallel with these metabolic and energetic restorations, the lesions in nuclear DNA were removed within 3 h; however, even after 24 h, lesions in mitochondrial DNA were only partially repaired. We have also found that the Chk1 pathway has a major role in the maintenance of genomic integrity following treatment with P-AscH-. Hence, combinations of P-AscH- and Chk1 inhibitors could have the potential to improve outcomes of cancer treatment. Hyperactivation of PARP-1 and DNA repair are ATP-consuming processes. Using a Seahorse XF96 Analyzer, we observed no changes in OCR or ECAR/PPR following treatment with P-AscH-. OCR and ECAR/PPR together indicate the rate of production of intracellular ATP; therefore, the rate of production is unchanged after challenge with P-AscH-. Thus, the severe decrease in ATP is due solely to increased demand. Genetic deletion and pharmacological inhibition of PARP-1 preserved both NAD+ and ATP; however, the toxicity of P-AscH- remained. These data indicate that loss of NAD+ and ATP are secondary factors in the toxicity of P-AscH-, and damage to DNA is the primary factor. These preclinical findings can guide the best use of P-AscH- as an adjuvant in cancer therapy.
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Doonan, Patrick John. "Mitochondrial Calcium Uptake: LETM1 and MICU1 Are Mitochondrial Proteins That Regulate Mitochondrial Calcium Homeostasis and Cellular Bioenergetics." Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214818.

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Biochemistry
Ph.D.
Mitochondrial calcium (Ca2+) uptake has been studied for over five decades, with crucial insights into its underlying mechanisms enabled by development of the chemi-osmotic hypothesis and appreciation of the considerable voltage present across the inner mitochondrial membrane (ΔΨm) generated by proton pumping by the respiratory chain (Carafoli, 1987; Nicholls, 2005). However, the molecules that regulate mitochondrial Ca2+ uptake have only recently been identified (Jiang et. al., 2009; Perocchi et. al., 2010) and further work was needed to clarify how these molecules regulate mitochondrial Ca2+ uptake. Leucine Zipper EF hand containing Transmembrane Protein 1 (LETM1) acts as a regulator of mitochondrial Ca2+ uptake distinct from the mitochondrial Ca2+ uniporter (MCU) pathway (Jiang et. al., 2009). However, a controversy exists regarding the function of LETM1 (Nowikovsky et. al., 2004). Therefore, I asked if LETM1 played a role in mitochondrial Ca2+ uptake and if LETM1 regulated cellular bioenergetics and basal autophagy. To further characterize mitochondrial calcium uptake, we asked how Mitochondrial Calcium Uptake 1 (MICU1) regulates MCU activity by quantifying basal mitochondrial Ca2+ and MCU uptake rates in MICU1 ablated cells. The following work characterizes the molecules that regulate mitochondrial Ca2+ uptake and their mechanistic function on decoding calcium signals. Since LETM1 is the Ca2+/H+ antiporter, I hypothesize that alterations in LETM1 expression and activity will decrease mitochondrial Ca2+ uptake and will result in impaired mitochondrial bioenergetics. As a regulator of free intracellular Ca2+, mitochondrial Ca2+ uptake and the orchestra of its regulatory molecules have been implicated in many human diseases. Mitochondria act both upstream by regulating cytosolic Ca2+ concentration and as downstream effectors that respond to Ca2+ signals. Recently, LETM1 was proposed as a mitochondrial Ca2+/H+ antiporter (Jiang et. al., 2009); however characterization of the functional role of LETM1-mediated Ca2+ transfer remained unstudied. Therefore the specific aims of this project were to determine how LETM1 regulates Ca2+ homeostasis and bioenergetics under physiological settings. Secondly, this project aimed to characterize how LETM1-dependent Ca2+ signaling regulates ROS production and autophagy. The data presented here confirmed that LETM1 knockdown significantly impairs mitochondrial Ca2+ uptake. Furthermore, in-depth approaches including either deletion of EF-hand or mutation of critical EF-hand residues (D676A D688KLETM1) impaired histamine (GPCR agonist)-induced mitochondrial Ca2+ uptake. Knockdown of LETM1 resulted in bioenergetic collapse and promoted LC3-positive multilamellar vesicle formation, indicative of autophagy induction. Interestingly, knockdown of LETM1 significantly reduced complex IV but not complex I and complex II-mediated oxygen consumption rate (OCR). In contrast, cellular NADH and mitochondrial membrane potential (ΔΨm) were unaltered in both control and LETM1 knockdown cells. LETM1 has been implicated in formation of the supercomplexes of the electron transport chain (Tamai et. al., 2008). In support, these studies show that LETM1 knockdown results in increased reactive oxygen species (ROS) production. These results for the first time demonstrate that LETM1 controls cellular bioenergetics through regulation of mitochondrial Ca2+ and ROS. MICU1 was identified as an essential regulator of the mitochondrial Ca2+ uniporter (Perocchi et. al., 2010). Therefore, this project specifically aimed to determine how MICU1 regulates the mitochondrial Ca2+ uniporter. Interestingly, the data presented here suggest that MICU1 is not necessary for uniporter activity. Instead, loss of MICU1 caused mitochondria to constitutively load Ca2+ at rest which resulted in a host of cellular phenotypes. This result led to further questions on how MICU1 knockdown affects cellular bioenergetics and if MICU1 is essential for cell survival under stress. MICU1 ablation influenced pyruvate dehydrogenase activity and ROS production. Subsequent investigations demonstrated that increased basal ROS left cells poised to ceramide-induced cell death thereby suggesting the role of MICU1 in cell survival. Collectively, the data presented here show that MICU1 is necessary to control constitutive mitochondrial Ca2+ uptake during rest. This work demonstrates that LETM1 regulates a distinct mode of mitochondrial Ca2+ uptake pathway whereas MICU1 controls mitochondrial Ca2+ uniporter activity. Further studies are required to uncover the potential role of these two mitochondrial-resident Ca2+ regulators in health and disease.
Temple University--Theses
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Kuffner, Kerstin [Verfasser], and Christian H. [Akademischer Betreuer] Wetzel. "Bioenergetics and Major Depressive Disorder - Investigations of Mitochondria Function in a Human Cellular Model / Kerstin Kuffner ; Betreuer: Christian H. Wetzel." Regensburg : Universitätsbibliothek Regensburg, 2020. http://d-nb.info/1214887007/34.

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Kim, Jaeyeon. "Model Analysis of Adipose Tissue and Whole Body Metabolism In Vivo." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1216436630.

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Hamraz, Minoo. "Bioenergetic consequences of the hyperosmotic shock." Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2332&f=17549.

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L'inflammation est associée à des modifications du métabolisme cellulaire avec une glycolyse (libération de lactate) accrue accompagnée d'une baisse de la phosphorylation oxydative mitochondriale. L'inflammation cause l'hyperosmolarité du milieu extracellulaire. Cette thèse examine les effets de l'hyperosmolarité sur le métabolisme énergétique cellulaire. Nous avons mesuré la consommation d'oxygène cellulaire (OCR) et la production d'acide (PPR) c'est à dire de lactate libéré dans le milieu extérieur avec deux approches expérimentales : l'oxygraphie haute résolution (O2k Oroboros instrument) pour l'OCR et l'analyseur de flux extracellulaires (Seahorse Agilent) pour l'OCR et le PPR. L'exposition de cellules à des conditions hyperosmolaires (600 mOsmoles au lieu de la valeur normale 300) cause une répression de la consommation d'oxygène qui s'établit en quelques minutes et dure des heures (indéfiniment?) et à la longue affecte la viabilité cellulaire. Cet effet a été retrouvé sur plusieurs types cellulaires: CHO (épithélium ovarien), HT29 (colonocytes), HEK293 (rein embryonnaire), SH-SY5Y (neuroblastome). Il est reproduit avec trois osmolytes différents: le mannitol, le polyéthylène glycol et le chlorure de sodium. Un stress osmotique plus modéré (450 mOsm) cause une même chute de la respiration mais de durée limitée (une-deux heures). Une recherche des mécanismes à l'origine de cette inhibition montre que l'hyperosmolarité altère la fonction mitochondriale de différentes manières. Un premier effet est une inhibition du système enzymatique de production d'ATP. En présence de glucose cette inhibition s'accompagne d'une importante augmentation de la glycolyse qui cause une inhibition mitochondriale supplémentaire qui repose sur l'amplification de l'effet Crabtree (inhibition de la respiration par le glucose) dont la cible sont les complexes respiratoires. En l'absence de glucose le turnover cellulaire e l'ATP est sérieusement diminué mais de façon inattendue la survie cellulaire est plutôt meilleure. Ces résultats posent la question de la contribution des conditions hyperosmotiques liées à l'inflammation dans l'établissement d'un profil métabolique de type inflammatoire
Metabolic alterations associated with inflammation include increased recruitment of glycolysis (lactate release) and repression of mitochondrial oxidative phosphorylation. Inflammation causes hyperosmolar conditions in the extracellular medium. This thesis examines the consequences of hyperosmolarity on cellular bioenergetics. For this purpose we measured the cellular oxygen consumption rate (OCR) and proton production rate (PPR) for lactate release in the external medium. Two methodologies were used the high-resolution respirometer (O2k Oroboros Instruments) for OCR and the extracellular flux analyzer (Seahorse, Agilent) for OCR and PPR. The exposure cells to hypertonic conditions (600 milliOsmoles while normal value is 300) causes within few minutes a decrease in OCR (cellular respiration) that lasts for hours (indefinitely) and in the long term impact on cellular viability. This effect was observed with four different cell lines CHO (ovarian epithelial), HT29 (colonocytes), HEK293 (Embryonic kidney) and SH-SY5Y (Neuroblastoma). It was shown to be caused by three different osmolytes: Mannitol, polyethylene glycol, sodium chloride. A milder osmotic challenge (450 mOsm) caused a similar initial decrease but with restoration of initial OCR within few hours. The mechanisms underlying this effect have been investigated, hyperosmolarity impacts on mitochondrial respiration at different steps. A first effect is the inhibition of the mitochondrial ATP production step. In presence of glucose this is accompanied by a large increase in glycolysis (lactate release) that causes further mitochondrial inhibition by a second mechanism, which is likely to represent an enhancement of the Crabtree effect (inhibition of respiration by glycolysis) that impacts on respiratory complexes. In absence of glucose the cellular ATP turnover is seriously repressed surprisingly cellular survival is rather improved. These results raise therefore the question of the possible contribution of the hyperosmotic conditions caused by inflammation in the acquisition of the inflammatory metabolic profile
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Wright, Muelas Marina. "A systems biology approach to cancer metabolism." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/a-systems-biology-approach-to-cancer-metabolism(27286c8a-0281-4256-b749-2ec9bd36370f).html.

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Cancer cells have been known for some time to have very different metabolismas compared to that of normal non proliferating cells. As metabolism is involvedin almost every aspect of cell function, there has been a recent resurgence ofinterest in inhibiting cancer metabolism as a therapeutic strategy. Inhibitors thatspecifically target altered metabolic components in cancer cells are being developedas antiproliferative agents. However, many such inhibitors have not progressedinto the clinic due to limited efficacy either in vitro or in vivo. In this study weexplore the hypothesis that this is often due to the robustness of the metabolicnetwork and the differences between individual cancer cell lines in their metaboliccharacteristics. We take a systems biology approach. We investigate the cellular bioenergetic profiles of a panel of five non-small celllung cancer cell lines before and after treatment with a novel inhibitor of theglutaminase-1 (GLS1) enzyme. Additionally, we explore the effects of this inhibitoron intracellular metabolism of these cell lines as well as on the uptake and secretionof glucose, lactate and amino acids. To be able to do the latter robustly, wehad to modify the experimental assay considerably from procedures that seemto be standard in the literature; using these earlier procedures the metabolicenvironment of the cells was highly variable, leading to misleading results onthe metabolic effects of the inhibitor. We reduced cell density, altered mediumvolume and changed the time-window of the assay. This led to the cells growingexponentially, appearing indifferent to the few remaining changes. In this newassay, the metabolic effects of the glutaminase inhibitor became robust. One of the most significant results of this study is the metabolic heterogeneitydisplayed across the cell line panel under basal conditions. Differences in themetabolic functioning of the cell lines were observed in terms of both theirbioenergetic and metabolic profile. The amount of respiration attributed tooxidative phosphorylation differed between cell lines and respiratory capacity wasattenuated in most cells. However, the rate of glycolysis was similar betweencell lines in this assay. These results suggest that the Warburg effect arisesthrough a greater diversity of mechanisms than traditionally assumed, involvingvarious combinations of changes in the expression of glycolytic and mitochondrialmetabolic enzymes. The effects of GLS1 inhibition on cellular bioenergetics and metabolism alsodiffered between cell lines, even between resistant cell lines, indicating that theremay also be a diversity of resistance mechanisms. The metabolomic response ofcell lines to treatment suggests potential resistance mechanisms through metabolicadaptation or through the prior differences in the metabolic function of resistantcell lines. Part of the metabolome response to GLS1 inhibition was quite specificfor sensitive cells, with high concentrations of IMP as the strongest marker. Our results suggest that the metabolome is a significant player in what determinesthe response of cells to metabolic inhibitors, that its responses differ between cancercells, that responses are not beyond systems understanding, and that thereforethe metabolome should be taken into account in the design of and therapy withanti-cancer drugs.
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Books on the topic "Cellular bioenergetics"

1

Papa, Sergio, Ferruccio Guerrieri, and Joseph M. Tager, eds. Frontiers of Cellular Bioenergetics. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0.

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Saks, Valdur A., and Renée Ventura-Clapier, eds. Cellular Bioenergetics: Role of Coupled Creatine Kinases. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2612-4.

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Nederkoorn, Paul H. J. Signal transduction by G protein-coupled receptors: Bioenergetics and G protein activation : proton transfer and GTP synthesis to explain the experimental findings. New York: Springer, 1997.

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Cramer, W. A. Energy transduction in biological membranes: A textbook of bioenergetics. New York: Springer-Verlag, 1990.

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Papa, S., Joseph M. Tager, and Ferruccio Guerrieri. Frontiers of Cellular Bioenergetics. Springer My Copy UK, 1999.

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Saks, V. A. Cellular Bioenergetics: Role of Coupled Creatine Kinases. Springer, 2012.

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A, Saks V., and Ventura-Clapier Renée, eds. Cellular bioenergetics: Role of coupled creatine kinases. Dordrecht: Kluwer Academic Publishers, 1994.

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(Editor), Valdur A. Saks, and Renée Ventura-Clapier (Editor), eds. Cellular Bioenergetics: Role of Coupled Creatine Kinases (Developments in Molecular and Cellular Biochemistry). Springer, 1994.

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S, Papa, Guerrieri Ferruccio, and Tager J. M, eds. Frontiers of cellular bioenergetics: Molecular biology, biochemistry, and physiopathology. New York: Kluwer Academic/Plenum Press, 1999.

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(Editor), S. Papa, Ferruccio Guerrieri (Editor), and Joseph M. Tager (Editor), eds. Frontiers of Cellular Bioenergetics: Molecular Biology, Biochemistry, and Physiopathology. Springer, 1999.

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Book chapters on the topic "Cellular bioenergetics"

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Ji, Sayer, and Ali Le Vere. "Revisioning Cellular Bioenergetics." In Nutrition and Integrative Medicine, 291–318. Boca Raton : Taylor & Francis, 2018.: CRC Press, 2018. http://dx.doi.org/10.1201/9781315153155-10.

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Stucki, Jörg W., and Erwin Sigel. "Nonequilibrium Thermodynamics and Cellular Bioenergetics." In Integration of Mitochondrial Function, 169–75. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_15.

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Giuffrè, Alessandro, Paolo Sarti, Emilio D’Itri, Gerhard Buse, Tewfik Soulimane, and Maurizio Brunori. "Transient Spectroscopy of the Reaction between Cytochrome c Oxidase and Nitric Oxide." In Frontiers of Cellular Bioenergetics, 219–32. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_10.

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Trumpower, Bernard L. "Energy Transduction in Mitochondrial Respiration by the Proton-Motive Q-Cycle Mechanism of the Cytochrome bc 1 Complex." In Frontiers of Cellular Bioenergetics, 233–61. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_11.

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Yu, Chang-An, Li Zhang, Anatoly M. Kachurin, Sudha K. Shenoy, Kai-Ping Deng, Linda Yu, Di Xia, Hoeon Kim, and Johann Deisenhofer. "The Crystal Structure of Mitochondrial Cytochrome bc 1 Complex." In Frontiers of Cellular Bioenergetics, 263–89. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_12.

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Link, Thomas A. "Structural Aspects of the Cytochrome bc 1 Complex." In Frontiers of Cellular Bioenergetics, 291–324. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_13.

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Schulte, Ulrich, and Hanns Weiss. "Structure, Function, and Biogenesis of Respiratory Complex I." In Frontiers of Cellular Bioenergetics, 325–60. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_14.

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Bianchet, Mario A., Peter L. Pedersen, and L. Mario Amzel. "Structure of F1 -ATPase and the Mechanism of ATP Synthesis— Hydrolysis." In Frontiers of Cellular Bioenergetics, 361–76. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_15.

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Souid, Abdul-Kader, and Harvey S. Penefsky. "Mechanism of ATP Synthesis by Mitochondrial ATP Synthase." In Frontiers of Cellular Bioenergetics, 377–98. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_16.

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Futai, Masamitsu, and Hiroshi Omote. "Mutational Analysis of ATP Synthase An Approach to Catalysis and Energy Coupling." In Frontiers of Cellular Bioenergetics, 399–421. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4843-0_17.

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Conference papers on the topic "Cellular bioenergetics"

1

Xu, Weiling, Suzy A. Comhair, Allison J. Janocha, Lori A. Mavrakis, and Serpil C. Erzurum. "Cellular Bioenergetics In Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2807.

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Biniecka, Monika, Emese Balogh, Aisling Kennedy, Chin T. Ng, Douglas J. Veale, and Ursula Fearon. "04.20 Oxidative stress alters cellular bioenergetics in inflammatory arthritis." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211051.20.

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Xu, Weiling, Suzy A. A. Comhair, Allison J. Janocha, Lori A. Mavrakis, and Serpil C. Erzurum. "Alteration Of Nitric Oxide Synthesis Related To Abnormal Cellular Bioenergetics In Asthmatic Airway Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1436.

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Chen, Shanwen, Pengyuan Wang, Yisheng Pan, and Yucun Liu. "Abstract 5840: Inhibition of cystathionine-β-synthase (CBS) sensitizes colon cancer cells to 5-FU via increasing apoptosis and inhibiting cellular bioenergetics." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5840.

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Ferreira, Rodrigo, Christian Maibohm, Oscar F. Silvestre, Rosa Romero, Helder Crespo, and Jana B. Nieder. "Few-Cycle Laser for the in Vitro Study of Cellular Bioenergetics during Therapeutic Treatment with the Anticancer Drug Doxorubicin in its Free and Liposomal Nanocarrier Form." In 2019 Conference on Lasers and Electro-Optics Europe & European Quantum Electronics Conference (CLEO/Europe-EQEC). IEEE, 2019. http://dx.doi.org/10.1109/cleoe-eqec.2019.8871603.

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Fan, Yongjun, Kathleen G. Dickman, and Wei‐Xing Zong. "Abstract B96: Akt and c‐Myc differentially activate cellular metabolic programs and prime cells to bioenergetic inhibition." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b96.

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