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Journal articles on the topic 'Cellular respiration'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Rannels, D. Eugene. "Cellular neurobiology of respiration." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 1 (July 1, 1995): L1. http://dx.doi.org/10.1152/ajplung.1995.269.1.l1.

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2

Chandel, Navdeep S., G. R. Scott Budinger, Sang H. Choe, and Paul T. Schumacker. "Cellular Respiration during Hypoxia." Journal of Biological Chemistry 272, no. 30 (July 25, 1997): 18808–16. http://dx.doi.org/10.1074/jbc.272.30.18808.

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3

Brunori, M., A. Giuffr�, P. Sarti, G. Stubauer, and M. T. Wilson. "Nitric oxide and cellular respiration." Cellular and Molecular Life Sciences (CMLS) 56, no. 7-8 (November 1, 1999): 549–57. http://dx.doi.org/10.1007/s000180050452.

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4

Jones, Eyone, Harvey S. Penefsky, and Abdul-Kader Souid. "Caffeine Impairs HL-60 Cellular Respiration." Journal of Medical Sciences 2, no. 2 (May 29, 2009): 61–72. http://dx.doi.org/10.2174/1996327000902020061.

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5

Tao, Zhimin, Matthew P. Morrow, Tewodros Asefa, Krishna K. Sharma, Cole Duncan, Abhishek Anan, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Mesoporous Silica Nanoparticles Inhibit Cellular Respiration." Nano Letters 8, no. 5 (May 2008): 1517–26. http://dx.doi.org/10.1021/nl080250u.

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6

Cascón, Alberto, Laura Remacha, Bruna Calsina, and Mercedes Robledo. "Pheochromocytomas and Paragangliomas: Bypassing Cellular Respiration." Cancers 11, no. 5 (May 16, 2019): 683. http://dx.doi.org/10.3390/cancers11050683.

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Pheochromocytomas and paragangliomas (PPGL) are rare neuroendocrine tumors that show the highest heritability of all human neoplasms and represent a paradoxical example of genetic heterogeneity. Amongst the elevated number of genes involved in the hereditary predisposition to the disease (at least nineteen) there are eleven tricarboxylic acid (TCA) cycle-related genes, some of which are also involved in the development of congenital recessive neurological disorders and other cancers such as cutaneous and uterine leiomyomas, gastrointestinal tumors and renal cancer. Somatic or germline mutation of genes encoding enzymes catalyzing pivotal steps of the TCA cycle not only disrupts cellular respiration, but also causes severe alterations in mitochondrial metabolite pools. These latter alterations lead to aberrant accumulation of “oncometabolites” that, in the end, may lead to deregulation of the metabolic adaptation of cells to hypoxia, inhibition of the DNA repair processes and overall pathological changes in gene expression. In this review, we will address the TCA cycle mutations leading to the development of PPGL, and we will discuss the relevance of these mutations for the transformation of neural crest-derived cells and potential therapeutic approaches based on the emerging knowledge of underlying molecular alterations.

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7

Tao, Zhimin, Henry G. Withers, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Inhibition of Cellular Respiration by Doxorubicin." Chemical Research in Toxicology 19, no. 8 (August 2006): 1051–58. http://dx.doi.org/10.1021/tx050315y.

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8

Alsamri, Mohammed T., Suleiman Al-Hammadi, Barira Islam, and Abdul-Kader Souid. "Zoledronic acid and bone cellular respiration." Journal of Bone and Mineral Metabolism 36, no. 4 (August 1, 2017): 392–98. http://dx.doi.org/10.1007/s00774-017-0850-7.

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9

Bishop, T., and M. D. Brand. "Processes contributing to metabolic depression in hepatopancreas cells from the snail Helix aspersa." Journal of Experimental Biology 203, no. 23 (December 1, 2000): 3603–12. http://dx.doi.org/10.1242/jeb.203.23.3603.

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Cells isolated from the hepatopancreas of the land snail Helix aspersa strongly depress respiration both immediately in response to lowered P(O2) (oxygen conformation) and, in the longer term, during aestivation. These phenomena were analysed by dividing cellular respiration into non-mitochondrial and mitochondrial respiration using the mitochondrial poisons myxothiazol, antimycin and azide. Non-mitochondrial respiration accounted for a surprisingly large proportion, 65+/−5 %, of cellular respiration in control cells at 70 % air saturation. Non-mitochondrial respiration decreased substantially as oxygen tension was lowered, but mitochondrial respiration did not, and the oxygen-conforming behaviour of the cells was due entirely to the oxygen-dependence of non-mitochondrial oxygen consumption. Non-mitochondrial respiration was still responsible for 45+/−2 % of cellular respiration at physiological oxygen tension. Mitochondrial respiration was further subdivided into respiration used to drive ATP turnover and respiration used to drive futile proton cycling across the mitochondrial inner membrane using the ATP synthase inhibitor oligomycin. At physiological oxygen tensions, 34+/−5 % of cellular respiration was used to drive ATP turnover and 22+/−4 % was used to drive proton cycling, echoing the metabolic inefficiency previously observed in liver cells from mammals, reptiles and amphibians. The respiration rate of hepatopancreas cells from aestivating snails was only 37 % of the control value. This was caused by proportional decreases in non-mitochondrial and mitochondrial respiration and in respiration to drive ATP turnover and to drive proton cycling. Thus, the fraction of cellular respiration devoted to different processes remained constant and the cellular energy balance was preserved in the hypometabolic state.

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10

Lobritz, Michael A., Peter Belenky, Caroline B. M. Porter, Arnaud Gutierrez, Jason H. Yang, Eric G. Schwarz, Daniel J. Dwyer, Ahmad S. Khalil, and James J. Collins. "Antibiotic efficacy is linked to bacterial cellular respiration." Proceedings of the National Academy of Sciences 112, no. 27 (June 22, 2015): 8173–80. http://dx.doi.org/10.1073/pnas.1509743112.

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Bacteriostatic and bactericidal antibiotic treatments result in two fundamentally different phenotypic outcomes—the inhibition of bacterial growth or, alternatively, cell death. Most antibiotics inhibit processes that are major consumers of cellular energy output, suggesting that antibiotic treatment may have important downstream consequences on bacterial metabolism. We hypothesized that the specific metabolic effects of bacteriostatic and bactericidal antibiotics contribute to their overall efficacy. We leveraged the opposing phenotypes of bacteriostatic and bactericidal drugs in combination to investigate their activity. Growth inhibition from bacteriostatic antibiotics was associated with suppressed cellular respiration whereas cell death from most bactericidal antibiotics was associated with accelerated respiration. In combination, suppression of cellular respiration by the bacteriostatic antibiotic was the dominant effect, blocking bactericidal killing. Global metabolic profiling of bacteriostatic antibiotic treatment revealed that accumulation of metabolites involved in specific drug target activity was linked to the buildup of energy metabolites that feed the electron transport chain. Inhibition of cellular respiration by knockout of the cytochrome oxidases was sufficient to attenuate bactericidal lethality whereas acceleration of basal respiration by genetically uncoupling ATP synthesis from electron transport resulted in potentiation of the killing effect of bactericidal antibiotics. This work identifies a link between antibiotic-induced cellular respiration and bactericidal lethality and demonstrates that bactericidal activity can be arrested by attenuated respiration and potentiated by accelerated respiration. Our data collectively show that antibiotics perturb the metabolic state of bacteria and that the metabolic state of bacteria impacts antibiotic efficacy.

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11

Henninger, D. D., D. N. Granger, and T. Y. Aw. "Enterocyte respiration rates in feline small intestine exposed to graded ischemia." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 1 (January 1, 1995): G116—G120. http://dx.doi.org/10.1152/ajpgi.1995.268.1.g116.

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The purpose of our study was to investigate the changes in enterocyte cellular and mitochondrial respiration rates subsequent to ischemia of graded duration. The small intestine of anesthetized adult cats was assigned to one of five treatment regimens: control or ischemia of 15-, 30-, 60-, or 90-min duration. Cellular and mitochondrial respiration was measured using a Clark-type O2 electrode at 0 and 4 h postharvest. Ischemia of increasing duration caused a progressive decrease in cellular and mitochondrial respiration in enterocytes at 0 h postharvest. By 4 h postharvest, cellular and mitochondrial respiration rates for the 15-, 30-, and 60-min ischemic groups had recovered to near control levels, whereas the 90-min group showed minimal recovery. These data suggest that ischemia suppresses cellular and mitochondrial respiration of intestinal epithelial cells, the magnitude of which is related to the ischemic duration. The ischemia-induced suppression in cellular respiration primarily reflects a reduction in mitochondrial respiration.

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12

Schumacker, P. T., N. Chandel, and A. G. Agusti. "Oxygen conformance of cellular respiration in hepatocytes." American Journal of Physiology-Lung Cellular and Molecular Physiology 265, no. 4 (October 1, 1993): L395—L402. http://dx.doi.org/10.1152/ajplung.1993.265.4.l395.

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Cellular respiratory rates are normally determined by metabolic activity, but become rate limited by O2 availability if the cell O2 tension (PO2) falls below a critical value (typically 1–10 Torr). An ability to reduce metabolic activity and energy demand in response to a falling O2 availability might confer an increased resistance to a diminished O2 supply. Isolated rat hepatocytes were studied in primary culture under controlled O2 tensions. Cells were obtained by collagenase digestion and seeded into nutritive media in control and experimental spinner flasks at identical cell densities. Cells subjected to rapid reduction in PO2 (100⇢0 Torr over < 40 min) exhibited undiminished O2 uptake until PO2 fell below 10 Torr. By contrast, when cell PO2 was reduced over several hours, significant decreases in O2 uptake became evident at O2 tensions as high as 70 Torr. These decreases were associated with a reduction in ATP concentration and an increase in NAD(P)H, compared with rapidly deoxygenated cells at the same PO2. No loss in cell viability was detected after 24 h at reduced PO2. The decrease in respiratory rate was associated with an increased rate of lactic acid production relative to normoxic controls. Restoration of normoxia was associated with an immediate return of O2 uptake to control levels. These results demonstrate that hepatocytes are capable of reversibly decreasing metabolic activity and O2 demand during sustained moderate reductions in PO2, via a mechanism that appears to involve an inhibition of mitochondrial function other than O2 supply limitation. This response may alter cellular susceptibility to physiological stresses including hypoxia.

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13

Jafri, M. Saleet, Stephen J. Dudycha, and Brian O'Rourke. "Cardiac Energy Metabolism: Models of Cellular Respiration." Annual Review of Biomedical Engineering 3, no. 1 (August 2001): 57–81. http://dx.doi.org/10.1146/annurev.bioeng.3.1.57.

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14

Wegrzyn, J., R. Potla, Y. J. Chwae, N. B. V. Sepuri, Q. Zhang, T. Koeck, M. Derecka, et al. "Function of Mitochondrial Stat3 in Cellular Respiration." Science 323, no. 5915 (February 6, 2009): 793–97. http://dx.doi.org/10.1126/science.1164551.

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15

Yip, Nga-Chi, Frankie J. Rawson, Chi Wai Tsang, and Paula M. Mendes. "Real-time electrocatalytic sensing of cellular respiration." Biosensors and Bioelectronics 57 (July 2014): 303–9. http://dx.doi.org/10.1016/j.bios.2014.01.059.

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16

Krycer, James R., Kelsey H. Fisher-Wellman, Daniel J. Fazakerley, Deborah M. Muoio, and David E. James. "Bicarbonate alters cellular responses in respiration assays." Biochemical and Biophysical Research Communications 489, no. 4 (August 2017): 399–403. http://dx.doi.org/10.1016/j.bbrc.2017.05.151.

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17

White, Joshua S., and April C. Maskiewicz. "Understanding Cellular Respiration in Terms of Matter & Energy within Ecosystems." American Biology Teacher 76, no. 6 (August 1, 2014): 408–14. http://dx.doi.org/10.1525/abt.2014.76.6.9.

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Using a design-based research approach, we developed a data-rich problem (DRP) set to improve student understanding of cellular respiration at the ecosystem level. The problem tasks engage students in data analysis to develop biological explanations. Several of the tasks and their implementation are described. Quantitative results suggest that students from the experimental class who participated in the DRP showed significant gains on cellular respiration posttest items, and students from the control class who participated in a non-DRP task showed no significant gains. Qualitative results from interviews and written responses showed that students from the experimental class progressed to deeper “levels of achievement” in cellular respiration. The data-rich tasks promote student understanding of cellular respiration, matter transformation, decomposition, and energy transformation – all goals recommended by the Next Generation Science Standards.

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18

Schröder, Lucie, Jennifer Senkler, and Hans-Peter Braun. "Special features of cellular respiration in Viscum album." Phytomedicine 61 (2019): 1. http://dx.doi.org/10.1016/j.phymed.2019.09.097.

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19

Souid, Abdul-Kader, Harvey S. Penefsky, Peter D. Sadowitz, and Bonnie Toms. "Enhanced Cellular Respiration in Cells Exposed to Doxorubicin†." Molecular Pharmaceutics 3, no. 3 (June 2006): 307–21. http://dx.doi.org/10.1021/mp050080j.

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20

Wikström, Mårten, Vivek Sharma, Ville R. I. Kaila, Jonathan P. Hosler, and Gerhard Hummer. "New Perspectives on Proton Pumping in Cellular Respiration." Chemical Reviews 115, no. 5 (February 19, 2015): 2196–221. http://dx.doi.org/10.1021/cr500448t.

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21

Brown, Mary H., and Reneè S. Schwartz. "Connecting photosynthesis and cellular respiration: Preservice teachers' conceptions." Journal of Research in Science Teaching 46, no. 7 (September 2009): 791–812. http://dx.doi.org/10.1002/tea.20287.

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22

Gnaiger, Erich, Rosmarie Steinlechner-Maran, Gabriela Méndez, Thomas Eberl, and Raimund Margreiter. "Control of mitochondrial and cellular respiration by oxygen." Journal of Bioenergetics and Biomembranes 27, no. 6 (December 1995): 583–96. http://dx.doi.org/10.1007/bf02111656.

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23

Maynard, Adam G., and Naama Kanarek. "NADH Ties One-Carbon Metabolism to Cellular Respiration." Cell Metabolism 31, no. 4 (April 2020): 660–62. http://dx.doi.org/10.1016/j.cmet.2020.03.012.

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24

De Abreu, Leiza Jane Lopes Lima, Valéria Sousa Melo, and Maria Izabel Gallão. "Quebra cabeça da respiração celular / Cellular respiration puzzle." Brazilian Journal of Development 7, no. 8 (August 13, 2021): 80729–38. http://dx.doi.org/10.34117/bjdv7n8-337.

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25

Neubauer, J. A., J. E. Melton, and N. H. Edelman. "Modulation of respiration during brain hypoxia." Journal of Applied Physiology 68, no. 2 (February 1, 1990): 441–51. http://dx.doi.org/10.1152/jappl.1990.68.2.441.

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This review is a summary of the effects of brain hypoxia on respiration with a particular emphasis on those studies relevant to understanding the cellular basis of these effects. Special attention is given to mechanisms that may be responsible for the respiratory depression that appears to be the primary sequela of brain hypoxia in animal models. Although a variety of potential mechanisms for hypoxic respiratory depression are considered, emphasis is placed on changes in the neuromodulator constituency of the respiratory neuron microenvironment during hypoxia as the primary cause of this phenomenon. Hypoxia is accompanied by a net increase in neuronal inhibition due to both decreased excitatory and increased inhibitory neuromodulator levels. A survey of hypoxia-tolerant cellular systems and organisms suggests that hypoxic respiratory depression may be a manifestation of the depression of cellular metabolism, which appears to be a major adaptation to limited oxygen availability in these systems.

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26

Sharanek, Ahmad, Audrey Burban, and Arezu Jahani-Asl. "CBMT-37. OSMR CONTROLS CELLULAR RESPIRATION AND RESISTANCE TO THERAPY." Neuro-Oncology 21, Supplement_6 (November 2019): vi41. http://dx.doi.org/10.1093/neuonc/noz175.159.

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Abstract Cytokines and their receptors play important roles in the regulation of cell fate, inflammation and immunity. The cytokine receptor for Oncostatin M (OSMR) drives brain tumor stem cell (BTSC) proliferation and tumorigenesis. Here, we report a novel role for OSMR in regulation of cellular respiration. Genetic knockdown of OSMR in BTSCs impairs mitochondrial biogenesis and oxidative phosphorylation. Importantly, blockade of OSMR signalling in BTSCs sensitizes them to ionizing radiation and Temozolomide in vitro and in vivo. This mechanism whereby OSMR regulates mitochondrial respiration and metabolism is conserved in post-mitotic neutrons. Thus, while OSMR is required for BTSC proliferation, OSMR confers resistance to therapy via enhancing mitochondrial respiration, independent of its role in proliferation. Our data suggest that therapeutic targeting of OSMR may be beneficial to eradicate quiescent tumour stem cells and tumour relapse.

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27

Whyte, Donna A., Suleiman Al-Hammadi, Ghazala Balhaj, Oliver M. Brown, Harvey S. Penefsky, and Abdul-Kader Souid. "Cannabinoids Inhibit Cellular Respiration of Human Oral Cancer Cells." Pharmacology 85, no. 6 (2010): 328–35. http://dx.doi.org/10.1159/000312686.

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28

Hill, G. E. "Cellular Respiration: The Nexus of Stress, Condition, and Ornamentation." Integrative and Comparative Biology 54, no. 4 (May 2, 2014): 645–57. http://dx.doi.org/10.1093/icb/icu029.

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29

D'Amico, G. "Inhibition of cellular respiration by endogenously produced carbon monoxide." Journal of Cell Science 119, no. 11 (May 9, 2006): 2291–98. http://dx.doi.org/10.1242/jcs.02914.

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30

Budin, Itay, Tristan de Rond, Yan Chen, Leanne Jade G. Chan, Christopher J. Petzold, and Jay D. Keasling. "Viscous control of cellular respiration by membrane lipid composition." Science 362, no. 6419 (October 25, 2018): 1186–89. http://dx.doi.org/10.1126/science.aat7925.

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Lipid composition determines the physical properties of biological membranes and can vary substantially between and within organisms. We describe a specific role for the viscosity of energy-transducing membranes in cellular respiration. Engineering of fatty acid biosynthesis inEscherichia coliallowed us to titrate inner membrane viscosity across a 10-fold range by controlling the abundance of unsaturated or branched lipids. These fluidizing lipids tightly controlled respiratory metabolism, an effect that can be explained with a quantitative model of the electron transport chain (ETC) that features diffusion-coupled reactions between enzymes and electron carriers (quinones). Lipid unsaturation also modulated mitochondrial respiration in engineered budding yeast strains. Thus, diffusion in the ETC may serve as an evolutionary constraint for lipid composition in respiratory membranes.

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31

Agrawal, Anurag, and Ulaganathan Mabalirajan. "Rejuvenating cellular respiration for optimizing respiratory function: targeting mitochondria." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 2 (January 15, 2016): L103—L113. http://dx.doi.org/10.1152/ajplung.00320.2015.

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Altered bioenergetics with increased mitochondrial reactive oxygen species production and degradation of epithelial function are key aspects of pathogenesis in asthma and chronic obstructive pulmonary disease (COPD). This motif is not unique to obstructive airway disease, reported in related airway diseases such as bronchopulmonary dysplasia and parenchymal diseases such as pulmonary fibrosis. Similarly, mitochondrial dysfunction in vascular endothelium or skeletal muscles contributes to the development of pulmonary hypertension and systemic manifestations of lung disease. In experimental models of COPD or asthma, the use of mitochondria-targeted antioxidants, such as MitoQ, has substantially improved mitochondrial health and restored respiratory function. Modulation of noncoding RNA or protein regulators of mitochondrial biogenesis, dynamics, or degradation has been found to be effective in models of fibrosis, emphysema, asthma, and pulmonary hypertension. Transfer of healthy mitochondria to epithelial cells has been associated with remarkable therapeutic efficacy in models of acute lung injury and asthma. Together, these form a 3R model—repair, reprogramming, and replacement—for mitochondria-targeted therapies in lung disease. This review highlights the key role of mitochondrial function in lung health and disease, with a focus on asthma and COPD, and provides an overview of mitochondria-targeted strategies for rejuvenating cellular respiration and optimizing respiratory function in lung diseases.

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32

Prince, Calais, Alina Maloyan, and Leslie Myatt. "Manipulation of TRKB activation alters cellular respiration in syncytiotrophoblasts." Placenta 45 (September 2016): 66–67. http://dx.doi.org/10.1016/j.placenta.2016.06.023.

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33

Liimatta, Erkki V., Axel Gödecke, Jürgen Schrader, and Ilmo E. Hassinen. "Regulation of cellular respiration in myoglobin-deficient mouse heart." Molecular and Cellular Biochemistry 256, no. 1/2 (January 2004): 201–8. http://dx.doi.org/10.1023/b:mcbi.0000009887.35254.61.

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34

Malvin, G. M., P. Havlen, and C. Baldwin. "Interactions between cellular respiration and thermoregulation in the paramecium." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R349—R352. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r349.

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An important adaptation to hypoxia is a regulated reduction in body temperature because it lowers metabolic rate when oxygen supply is limited. Although this beneficial response occurs in organisms ranging from protozoans to mammals, little is known of the cellular mechanisms responsible for the hypoxia-induced reduction in temperature. Using the unicellular protozoan, Paramecium caudatum, we showed that inhibition of oxidative phosphorylation with sodium azide (NaN3) under normoxic conditions mimics the thermoregulatory effects of hypoxia, causing this species to select a lower temperature in a thermal gradient (P < 0.0001). Under control conditions, selected temperature (Tsel) was 28.3 +/- 0.3 degrees C. NaN3 concentrations of 0.1 mM and above significantly reduced Tsel (P < 0.0001). Ten millimolar NaN3 produced the maximal reduction in Tsel, 11.4 degrees C, and the dose that produced 50% of the maximal response was 0.7 mM. The reduction in temperature was beneficial because both O2 consumption and survival were significantly less affected by NaN3 at lower temperatures. These results suggest that O2 does not directly affect thermoregulation in the paramecium. Rather, the hypoxia-induced reduction in Tsel results from inhibition of oxidative phosphorylation.

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35

Tao, Zhimin, Syed S. Ahmad, Harvey S. Penefsky, Jerry Goodisman, and Abdul-Kader Souid. "Dactinomycin Impairs Cellular Respiration and Reduces Accompanying ATP Formation." Molecular Pharmaceutics 3, no. 6 (December 2006): 762–72. http://dx.doi.org/10.1021/mp0600485.

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36

Yang, Tsanyen. "Mechanism of nitrite inhibition of cellular respiration inPseudomonas aeruginosa." Current Microbiology 12, no. 1 (January 1985): 35–39. http://dx.doi.org/10.1007/bf01567751.

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37

Wegrzyn, Joanna, Ramesh Potla, Yong-Joon Chwae, Qifang Zhang, Marta Derecka, Karol Szczepanek, Magdalena Szelag, et al. "372 A novel function of STAT3 in cellular respiration." Cytokine 43, no. 3 (September 2008): 331. http://dx.doi.org/10.1016/j.cyto.2008.07.457.

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38

Ojha, Krishna, John Ertle, and Michael C. Konopka. "Single Cell Examination of Membrane Fluidity and Cellular Respiration." Biophysical Journal 112, no. 3 (February 2017): 150a. http://dx.doi.org/10.1016/j.bpj.2016.11.820.

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39

Jeger, Victor, Sebastian Brandt, Francesca Porta, Stephan M. Jakob, Jukka Takala, and Siamak Djafarzadeh. "Dose Response of Endotoxin on Hepatocyte and Muscle Mitochondrial Respiration In Vitro." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/353074.

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Introduction.Results on mitochondrial dysfunction in sepsis are controversial. We aimed to assess effects of LPS at wide dose and time ranges on hepatocytes and isolated skeletal muscle mitochondria.Methods.Human hepatocellular carcinoma cells (HepG2) were exposed to placebo or LPS (0.1, 1, and 10 μg/mL) for 4, 8, 16, and 24 hours and primary human hepatocytes to 1 μg/mL LPS or placebo (4, 8, and 16 hours). Mitochondria from porcine skeletal muscle samples were exposed to increasing doses of LPS (0.1–100 μg/mg) for 2 and 4 hours. Respiration rates of intact and permeabilized cells and isolated mitochondria were measured by high-resolution respirometry.Results.In HepG2 cells, LPS reduced mitochondrial membrane potential and cellular ATP content but did not modify basal respiration. Stimulated complex II respiration was reduced time-dependently using 1 μg/mL LPS. In primary human hepatocytes, stimulated mitochondrial complex II respiration was reduced time-dependently using 1 μg/mL LPS. In isolated porcine skeletal muscle mitochondria, stimulated respiration decreased at high doses (50 and 100 μg/mL LPS).Conclusion.LPS reduced cellular ATP content of HepG2 cells, most likely as a result of the induced decrease in membrane potential. LPS decreased cellular and isolated mitochondrial respiration in a time-dependent, dose-dependent and complex-dependent manner.

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40

Gomez, Noe A. "The Fire of Life." American Biology Teacher 83, no. 7 (September 1, 2021): 479–81. http://dx.doi.org/10.1525/abt.2021.83.7.479.

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Teaching cellular respiration in the secondary classroom requires a carefully crafted approach. The discipline, though complex, represents the cornerstone of cellular metabolic transactions. Therefore, this article proposes a method to engage students in the subject through an agricultural lens. Specifically, this will be done by having students consider why animals eat feed and where feed energy goes. After developing an appreciation for such feeding dynamics in animals, students will be better suited for studying the molecular nature of cellular respiration.

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41

Avram, Vlad F., Imen Chamkha, Eleonor Åsander-Frostner, Johannes K. Ehinger, Romulus Z. Timar, Magnus J. Hansson, Danina M. Muntean, and Eskil Elmér. "Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Statin Toxicity." International Journal of Molecular Sciences 22, no. 1 (January 3, 2021): 424. http://dx.doi.org/10.3390/ijms22010424.

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Statins are the cornerstone of lipid-lowering therapy. Although generally well tolerated, statin-associated muscle symptoms (SAMS) represent the main reason for treatment discontinuation. Mitochondrial dysfunction of complex I has been implicated in the pathophysiology of SAMS. The present study proposed to assess the concentration-dependent ex vivo effects of three statins on mitochondrial respiration in viable human platelets and to investigate whether a cell-permeable prodrug of succinate (complex II substrate) can compensate for statin-induced mitochondrial dysfunction. Mitochondrial respiration was assessed by high-resolution respirometry in human platelets, acutely exposed to statins in the presence/absence of the prodrug NV118. Statins concentration-dependently inhibited mitochondrial respiration in both intact and permeabilized cells. Further, statins caused an increase in non-ATP generating oxygen consumption (uncoupling), severely limiting the OXPHOS coupling efficiency, a measure of the ATP generating capacity. Cerivastatin (commercially withdrawn due to muscle toxicity) displayed a similar inhibitory capacity compared with the widely prescribed and tolerable atorvastatin, but did not elicit direct complex I inhibition. NV118 increased succinate-supported mitochondrial oxygen consumption in atorvastatin/cerivastatin-exposed platelets leading to normalization of coupled (ATP generating) respiration. The results acquired in isolated human platelets were validated in a limited set of experiments using atorvastatin in HepG2 cells, reinforcing the generalizability of the findings.

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42

Saat, Rohaida Mohd, Hidayah Mohd Fadzil, Nor Azlina Abd. Aziz, Kamariah Haron, Kamaludin A. Rashid, and Natalya Rudina Shamsuar. "DEVELOPMENT OF AN ONLINE THREE-TIER DIAGNOSTIC TEST TO ASSESS PRE-UNIVERSITY STUDENTS’ UNDERSTANDING OF CELLULAR RESPIRATION." Journal of Baltic Science Education 15, no. 4 (August 25, 2016): 532–46. http://dx.doi.org/10.33225/jbse/16.15.532.

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This research reports the development of an online three-tier diagnostic instrument for pre-university students related to cellular respiration. To date, only few studies have been conducted to identify students’ alternative conception in the topic of cellular respiration. One of the contributing factors is due to lack of instrument developed to measure these alternative conceptions. Three-tier tests are used as assessment tools for lecturers to determine students’ alternative conceptions related to cellular respiration and their knowledge and understanding about the concepts. The research incorporates both qualitative and quantitative methods. The instrument was developed in five phases: (1) construction of items, (2) pilot study, (3) validation of instrument, (4) transforming the instrument into an online assessment tool, and (5) the administration of the Online Diagnostic Tool (ODiT). The Cellular Respiration ODiT consists of three tiers: answer and reasoning tiers to measure “content knowledge” and “explanatory knowledge” respectively, and a third tier that measures the level of confidence of pre-university students. Analysis of the students’ responses demonstrated acceptable reliability and validity of the instrument. The research also shows that both students and lecturers benefit when online diagnostic tests are implemented appropriately. Key words: biology alternative conception, online diagnostic tool, three-tier diagnostic test.

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Mishra, Jay S., Chellakkan S. Blesson, and Sathish Kumar. "Testosterone Decreases Placental Mitochondrial Content and Cellular Bioenergetics." Biology 9, no. 7 (July 20, 2020): 176. http://dx.doi.org/10.3390/biology9070176.

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Placental mitochondrial dysfunction plays a central role in the pathogenesis of preeclampsia. Since preeclampsia is a hyperandrogenic state, we hypothesized that elevated maternal testosterone levels induce damage to placental mitochondria and decrease bioenergetic profiles. To test this hypothesis, pregnant Sprague–Dawley rats were injected with vehicle or testosterone propionate (0.5 mg/kg/day) from gestation day (GD) 15 to 19. On GD20, the placentas were isolated to assess mitochondrial structure, copy number, ATP/ADP ratio, and biogenesis (Pgc-1α and Nrf1). In addition, in vitro cultures of human trophoblasts (HTR-8/SVneo) were treated with dihydrotestosterone (0.3, 1.0, and 3.0 nM), and bioenergetic profiles using seahorse analyzer were assessed. Testosterone exposure in pregnant rats led to a 2-fold increase in plasma testosterone levels with an associated decrease in placental and fetal weights compared with controls. Elevated maternal testosterone levels induced structural damage to the placental mitochondria and decreased mitochondrial copy number. The ATP/ADP ratio was reduced with a parallel decrease in the mRNA and protein expression of Pgc-1α and Nrf1 in the placenta of testosterone-treated rats compared with controls. In cultured trophoblasts, dihydrotestosterone decreased the mitochondrial copy number and reduced PGC-1α, NRF1 mRNA, and protein levels without altering the expression of mitochondrial fission/fusion genes. Dihydrotestosterone exposure induced significant mitochondrial energy deficits with a dose-dependent decrease in basal respiration, ATP-linked respiration, maximal respiration, and spare respiratory capacity. In summary, our study suggests that the placental mitochondrial dysfunction induced by elevated maternal testosterone might be a potential mechanism linking preeclampsia to feto-placental growth restriction.

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Marcinek, David J., Wayne A. Ciesielski, Kevin E. Conley, and Kenneth A. Schenkman. "Oxygen regulation and limitation to cellular respiration in mouse skeletal muscle in vivo." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 5 (November 2003): H1900—H1908. http://dx.doi.org/10.1152/ajpheart.00192.2003.

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In skeletal muscle, intracellular Po2 can fall to as low as 2–3 mmHg. This study tested whether oxygen regulates cellular respiration in this range of oxygen tensions through direct coupling between phosphorylation potential and intracellular Po2. Oxygen may also behave as a simple substrate in cellular respiration that is near saturating levels over most of the physiological range. A novel optical spectroscopic method was used to measure tissue oxygen consumption (Ṁo2) and intracellular Po2 using the decline in hemoglobin and myoglobin saturation in the ischemic hindlimb muscle of Swiss-Webster mice. 31P magnetic resonance spectroscopic determinations yielded phosphocreatine concentration ([PCr]) and pH in the same muscle volume. Intracellular Po2 fell to <2 mmHg during the ischemic period without a change in the muscle [PCr] or pH. The constant phosphorylation state despite the decline in intracellular Po2 rejects the hypothesis that direct coupling between these two variables results in a regulatory role for oxygen in cellular respiration. A second set of experiments tested the relationship between intracellular Po2 and Ṁo2. In vivo Ṁo2 in mouse skeletal muscle was increased by systemic treatment with 2 and 4 mg/kg body wt 2,4-dinitrophenol to partially uncouple mitochondria. Ṁo2 was not dependent on intracellular Po2 above 3 mmHg in the three groups despite a threefold increase in Ṁo2. These results indicate that Ṁo2 and the phosphorylation state of the cell are independent of intracellular Po2 throughout the physiological range of oxygen tensions. Therefore, we reject a regulatory role for oxygen in cellular respiration and conclude that oxygen acts as a simple substrate for respiration under physiological conditions.

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Lucas, Stephanie, Guohua Chen, Siddhesh Aras, and Jian Wang. "Serine catabolism is essential to maintain mitochondrial respiration in mammalian cells." Life Science Alliance 1, no. 2 (May 2018): e201800036. http://dx.doi.org/10.26508/lsa.201800036.

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Breakdown of serine by the enzyme serine hydroxymethyltransferase (SHMT) produces glycine and one-carbon (1C) units. These serine catabolites provide important metabolic intermediates for the synthesis of nucleotides, as well as methyl groups for biosynthetic and regulatory methylation reactions. Recently, it has been shown that serine catabolism is required for efficient cellular respiration. Using CRISPR-Cas9 gene editing, we demonstrate that the mitochondrial SHMT enzyme, SHMT2, is essential to maintain cellular respiration, the main process through which mammalian cells acquire energy. We show that SHMT2 is required for the assembly of Complex I of the respiratory chain. Furthermore, supplementation of formate, abona fide1C donor, restores Complex I assembly in the absence of SHMT2. Thus, provision of 1C units by mitochondrial serine catabolism is critical for cellular respiration, at least in part by influencing the assembly of the respiratory apparatus.

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O'Connell, Dan. "An Inquiry-based Approach to Teaching Photosynthesis & Cellular Respiration." American Biology Teacher 70, no. 6 (August 2008): 350–56. http://dx.doi.org/10.1662/0002-7685(2008)70[350:aiattp]2.0.co;2.

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O'Connell, Dan. "An Inquiry-Based Approach to Teaching Photosynthesis & Cellular Respiration." American Biology Teacher 70, no. 6 (August 1, 2008): 350–56. http://dx.doi.org/10.2307/30163295.

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Quirk, P. G., M. R. Jones, R. S. Haworth, R. B. Beechey, and I. D. Campbell. "Uncoupler Resistance in Escherichia coli: the Role of Cellular Respiration." Microbiology 135, no. 10 (October 1, 1989): 2577–87. http://dx.doi.org/10.1099/00221287-135-10-2577.

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Presley, Tennille, C. D. Venkatakrishnan, Anna Bratasz, Periannan Kuppusamy, and Govindasamy Ilangovan. "P016. EPR oximetry to demonstrate NO inhibition of cellular respiration." Nitric Oxide 14, no. 4 (June 2006): 22. http://dx.doi.org/10.1016/j.niox.2006.04.075.

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Du, Lin, Fakhri Mahdi, Mika B. Jekabsons, Dale G. Nagle, and Yu-Dong Zhou. "Natural and Semisynthetic Mammea-Type Isoprenylated Dihydroxycoumarins Uncouple Cellular Respiration." Journal of Natural Products 74, no. 2 (February 25, 2011): 240–48. http://dx.doi.org/10.1021/np100762s.

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