Journal articles: 'Cell respiration'

1

Harborne, Jeffrey B. "Higher plant cell respiration." Phytochemistry 25, no. 6 (May 1986): 1515. http://dx.doi.org/10.1016/s0031-9422(00)81331-x.

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Black, Clanton C. "Plant Respiration Higher Plant Cell Respiration R. Douce D. A. Day." BioScience 37, no. 10 (November 1987): 742–43. http://dx.doi.org/10.2307/1310486.

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Li, Ding, Zhexu Ding, Manjin Gui, Yanmei Hou, and Kui Xie. "Metabolic Enhancement of Glycolysis and Mitochondrial Respiration Are Essential for Neuronal Differentiation." Cellular Reprogramming 22, no. 6 (December 1, 2020): 291–99. http://dx.doi.org/10.1089/cell.2020.0034.

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Garmash, E. V. "Mitochondrial respiration of the photosynthesizing cell." Russian Journal of Plant Physiology 63, no. 1 (January 2016): 13–25. http://dx.doi.org/10.1134/s1021443715060072.

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SIEDOW, J. N. "Plant Mitochondria: Higher Plant Cell Respiration." Science 230, no. 4723 (October 18, 1985): 313–14. http://dx.doi.org/10.1126/science.230.4723.313.

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Mawson, B. T. "Cyanide-resistant, alternative pathway respiration in guard cell protoplasts of Vicia faba." Canadian Journal of Botany 72, no. 2 (February 1, 1994): 150–56. http://dx.doi.org/10.1139/b94-020.

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The activity and capacity of cyanide-resistant or alternative pathway respiration was examined in Vicia faba L. guard and mesophyll cell protoplasts maintained either in darkness (dark adapted) or illuminated with blue light. Respiration rates by dark-adapted guard cell protoplasts were unaffected by titrating with salicylhydroxamic acid (0.1–2.0 mM), an inhibitor of alternative pathway respiration, suggesting the lack of activity of this pathway. In combination with 0.1 mM KCN, an inhibitor of cytochrome pathway respiration, salicylhydroxamic acid was effective in inhibiting total respiration rates. In contrast with guard cell protoplasts, salicylhydroxamic acid reduced rates of O2 consumption in dark-adapted mesophyll cell protoplasts by 25–30% of total respiration. Titrating the cytochrome pathway of guard cell protoplasts with KCN (10–140 μM) alone failed to reduce respiratory activity but was effective in combination with salicylhydroxamic acid. Addition of a proton ionophore, carbonyl cyanide m-chlorophenylhydraxone, to dark-adapted guard cell protoplast suspensions increased respiration by approximately 30 and 84% in the presence and absence of salicylhydroxamic acid, suggesting restriction of electron flow by adenylates. Illumination of guard cell protoplasts with blue light for 30 min increased the sensitivity of respiration to salicylhydroxamic acid and increased the activity of the alternative pathway over this time period to ~55% of total respiration. Blue light also increased the rate of uncoupled respiration by guard cell protoplasts treated with salicylhydroxamic acid compared with dark-adapted protoplasts. The results suggest that electron movement through either cytochrome or alternative pathways in guard cell mitochondria may be regulated during signal transduction of blue light. Key words: Vicia faba, guard cell protoplasts, alternative pathway, respiration, blue light.

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MacDonald, J. R., M. Oellermann, S. Rynbeck, G. Chang, K. Ruggiero, G. J. S. Cooper, and A. J. R. Hickey. "Transmural differences in respiratory capacity across the rat left ventricle in health, aging, and streptozotocin-induced diabetes mellitus: evidence that mitochondrial dysfunction begins in the subepicardium." American Journal of Physiology-Cell Physiology 300, no. 2 (February 2011): C246—C255. http://dx.doi.org/10.1152/ajpcell.00294.2010.

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In diabetic cardiomyopathy, ventricular dysfunction occurs in the absence of hypertension or atherosclerosis and is accompanied by altered myocardial substrate utilization and depressed mitochondrial respiration. It is not known if mitochondrial function differs across the left ventricular (LV) wall in diabetes. In the healthy heart, the inner subendocardial region demonstrates higher rates of blood flow, oxygen consumption, and ATP turnover compared with the outer subepicardial region, but published transmural respirometric measurements have not demonstrated differences. We aim to measure mitochondrial function in Wistar rat LV to determine the effects of age, streptozotocin-diabetes, and LV layer. High-resolution respirometry measured indexes of respiration in saponin-skinned fibers dissected from the LV subendocardium and subepicardium of 3-mo-old rats after 1 mo of streptozotocin-induced diabetes and 4-mo-old rats following 2 mo of diabetes. Heart rate and heartbeat duration were measured under isoflurane-anesthesia using a fetal-Doppler, and transmission electron microscopy was employed to observe ultrastructural differences. Heart rate decreased with age and diabetes, whereas heartbeat duration increased with diabetes. While there were no transmural respirational differences in young healthy rat hearts, both myocardial layers showed a respiratory depression with age (30–40%). In 1-mo diabetic rat hearts only subepicardial respiration was depressed, whereas after 2 mo diabetes, respiration in subendocardial and subepicardial layers was depressed and showed elevated leak (state 2) respiration. These data provide evidence that mitochondrial dysfunction is first detectable in the subepicardium of diabetic rat LV, whereas there are measureable changes in LV mitochondria after only 4 mo of aging.

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Alfatni, Abrar, Anne-Laure Charles, François Sauer, Marianne Riou, Fabienne Goupilleau, Samy Talha, Alain Meyer, et al. "Peripheral Blood Mononuclear Cells Mitochondrial Respiration and Superoxide Anion after Heart Transplantation." Journal of Clinical Medicine 11, no. 23 (December 6, 2022): 7247. http://dx.doi.org/10.3390/jcm11237247.

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Introduction: The mitochondrial function of circulating peripheral blood mononuclear cells (PBMCs) is an interesting new approach to cardiac diseases. Thus, PBMC’s mitochondrial respiration decreases in relation to heart failure severity. However, no data are available on heart-transplanted patients (Htx). Population and Methods: We determined PBMCs mitochondrial respiration by high-resolution respirometry (Oroboros Instruments) and superoxide anion production using electron paramagnetic resonance (Bruker-Biospin) in 20 healthy subjects and 20 matched Htx and investigated clinical, biological, echocardiographic, coronarography and biopsy characteristics. Results: PBMCs mitochondrial respiratory chain complex II respiration was decreased in Htx (4.69 ± 0.84 vs. 7.69 ± 1.00 pmol/s/million cell in controls and Htx patients, respectively; p = 0.007) and complex IV respiration was increased (24.58 ± 2.57 vs. 15.68 ± 1.67 pmol/s/million cell; p = 0.0035). Superoxide anion production was also increased in Htx (1.47 ± 0.10 vs. 1.15 ± 0.10 µmol/min; p = 0.041). The leucocyte-to-lymphocyte ratio was increased in Htx, whom complex II correlated with leucocyte number (r = 0.51, p = 0.02) and with the left ventricular posterior wall peak early diastolic myocardial velocity (r = −0.62, p = 0.005). Complex IV was increased in the two patients with acute rejection and correlated negatively with Htx’s isovolumetric relation time (r = −0.45, p = 0.045). Discussion: Although presenting with normal systolic function, Htx demonstrated abnormal PBMC’s mitochondrial respiration. Unlike immunosuppressive therapies, subclinical diastolic dysfunction might be involved in these changes. Additionally, lymphopenia might reduce complex II, and acute rejection enhances complex IV respirations. Conclusion: PBMC’s mitochondrial respiration appears modified in Htx, potentially linked to cellular shift, mild diastolic dysfunction and/or acute rejection.

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Owiredu, Shawn, Abhay Ranganathan, David M. Eckmann, Frances S. Shofer, Kevin Hardy, David S. Lambert, Matthew Kelly, and David H. Jang. "Ex vivo use of cell-permeable succinate prodrug attenuates mitochondrial dysfunction in blood cells obtained from carbon monoxide-poisoned individuals." American Journal of Physiology-Cell Physiology 319, no. 1 (July 1, 2020): C129—C135. http://dx.doi.org/10.1152/ajpcell.00539.2019.

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The purpose of this study was to evaluate a new pharmacological strategy using a first-generation succinate prodrug, NV118, in peripheral blood mononuclear cells (PBMCs) obtained from subjects with carbon monoxide (CO) poisoning and healthy controls. We obtained human blood cells from subjects with CO poisoning and healthy control subjects. Intact PBMCs from subjects in the CO and Control group were analyzed with high-resolution respirometry measured in pmol O2 per second per 10−6 PBMCs. In addition to obtaining baseline respiration, NV118 (100 μM) was injected, and the same parameters of respiration were obtained for comparison in PBMCs. We measured mitochondrial dynamics with microscopy with the same conditions. We enrolled 37 patients (17 in the CO group and 20 in the Control group for comparison) in the study. PMBCs obtained from subjects in the CO group had overall significantly lower respiration compared with the Control group ( P < 0.0001). There was a significant increase in respiration with NV118, specifically with an increase in maximum respiration and respiration from complex II and complex IV ( P < 0.0001). The mitochondria in PBMCs demonstrated an overall increase in net movement compared with the Control group. Our results of this study suggest that the therapeutic compound, NV118, increases respiration at complex II and IV as well as restoration of mitochondrial movement in PBMCs obtained from subjects with CO poisoning. Mitochondrial-directed therapy offers a potential future strategy with further exploration in vivo.

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Nowak, Grazyna, and Diana Bakajsova. "Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells." American Journal of Physiology-Renal Physiology 303, no. 4 (August 15, 2012): F515—F526. http://dx.doi.org/10.1152/ajprenal.00072.2012.

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We demonstrated that nonselective PKC activation promotes mitochondrial function in renal proximal tubular cells (RPTC) following toxicant injury. However, the specific PKC isozyme mediating this effect is unknown. This study investigated the role of PKC-α in the recovery of mitochondrial functions in oxidant-injured RPTC. Wild-type PKC-α (wtPKC-α) and inactive PKC-α mutants were overexpressed in RPTC to selectively increase or block PKC-α activation. Oxidant ( tert-butyl hydroperoxidel; TBHP) exposure activated PKC-α in RPTC but decreased PKC-α levels in mitochondria following treatment. Uncoupled and state 3 respirations and activities of complexes I and IV in TBHP-injured cells decreased to 55, 44, 49, and 65% of controls, respectively. F0F1-ATPase activity and ATP content in injured RPTC decreased to 59 and 60% of controls, respectively. Oxidant exposure increased reactive oxygen species (ROS) production by 210% and induced mitochondrial fragmentation and 52% RPTC lysis. Overexpressing wtPKC-α did not block TBHP-induced ROS production but improved respiration and complex I activity, restored complex IV and F0F1-ATPase activities, promoted recovery of ATP content, blocked mitochondrial fragmentation, and reduced RPTC lysis to 14%. In contrast, inhibiting PKC-α 1) induced mitochondrial hyperpolarization and fragmentation; 2) blocked increases in ROS production; 3) prevented recovery of respiratory complexes and F0F1-ATPase activities, respiration, and ATP content; and 4) exacerbated TBHP-induced RPTC lysis. We conclude that 1) activation of PKC-α prevents mitochondrial hyperpolarization and fragmentation, decreases cell death, and promotes recovery of mitochondrial respiration and ATP content following oxidant injury in RPTC; and 2) respiratory complexes I and IV and F0F1-ATPase are targets of active PKC-α.

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11

Verkhovsky, Michael I., Joel E. Morgan, Anne Puustinen, and Mårten Wikström. "Kinetic trapping of oxygen in cell respiration." Nature 380, no. 6571 (March 1996): 268–70. http://dx.doi.org/10.1038/380268a0.

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12

Schulz, Hans-Ulrich, Matthias Pross, Frank Meyer, Rainer Matthias, and Walter Halangk. "ACINAR CELL RESPIRATION IN EXPERIMENTAL ACUTE PANCREATITIS." SHOCK 3, no. 3 (March 1995): 184–88. http://dx.doi.org/10.1097/00024382-199503000-00005.

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13

E, Bon, Maksimovich N.Ye, and Dremza I.K. "Methodological Approaches to the Study of Mitochondrial Respiration." Journal of Clinical Case Reports and Studies 3, no. 3 (March 26, 2022): 01–06. http://dx.doi.org/10.31579/2690-8808/108.

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Energy exchange in the cell is associated with mitochondria, which play an important role in vital processes. The Oxidative Phosphorylation System (OxРhoS), localized in the inner mitochondrial membrane, consists of five membrane enzymes. Four of the five protein complexes make up the "respiratory chain" and are involved in the transfer of electrons, which at three points is coupled with the translocation of protons across the inner mitochondrial membrane. The resulting proton gradient is used by the ATP synthase complex (the fifth enzyme complex) to phosphorylate ADP. The methods for studying the activity of the electron transport chain of mitochondria described in the article, especially their use in a complex, makes it possible to significantly detail the understanding of the pathogenesis of disorders of cell energy exchange that occurs in various diseases, which will improve the prevention and correction of mitochondrial dysfunction.

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14

Govindjee. "Advances in Photosynthesis and Respiration: Focus on Plant Respiration." Photosynthesis Research 85, no. 2 (August 2005): 255–59. http://dx.doi.org/10.1007/s11120-005-4919-0.

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15

Strzyz, Paulina. "ER stress boosts respiration." Nature Reviews Molecular Cell Biology 20, no. 8 (May 3, 2019): 453. http://dx.doi.org/10.1038/s41580-019-0139-x.

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Asami, Kouichi. "‘A century homework,’: how fertilisation causes elevation of respiration in the sea urchin egg." Zygote 8, S1 (December 1999): S5—S6. http://dx.doi.org/10.1017/s0967199400130023.

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The lecture given by Dr Yasumasu should be considered from two points of view, namely its significance in the field of developmental biology and his own personal history as a developmental biologist.In 1908 Otto Warburg published a paper entitled ‘Beobachtungen üeber die Oxydationsprozesse im Seeigelei’ (Warburg, 1908). This is one of his earliest works, where he measured respiration of eggs with Winkler's method not with his manometer. This was the first paper describing the fact that the respiration in unfertilised eggs was considerably lower than that in fertilised ones. Many researchers confirmed his experiments and extended them. Borei (1948) measured oxygen consumption of oocytes and unfertilised and fertilised eggs and compared his results with those of other researchers. He observed that the respiration of eggs declined after they were removed from the ovary and placed into seawater and that it increased at fertilisation. He observed an exponential increase in respiration of fertilised eggs or embryos from the cleavage stage to the hatching blastula. He also observed an initial burst of respiration but failed to record it exactly. Ohnishi & Sugiyama (1963) measured the initial burst of respiration quantitatively with the oxygen electrode method. Thus, respiration of sea urchin eggs and early embryos was divided into three phases: respiration of unfertilised eggs, the initial burst of respiration at fertilisation and the respiration of fertilised eggs. The respiration of fertilised eggs increased exponentially with progression of development until hatching.

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Lu, Zhenmin, Miguel A. Quiñones, and Eduardo Zeiger. "Temperature dependence of guard cell respiration and stomatal conductance co-segregate in an F2 population of Pima cotton." Functional Plant Biology 27, no. 5 (2000): 457. http://dx.doi.org/10.1071/pp98128.

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In Pima cotton (Gossypium barbadense L.), stomatal conductance shows a strong response to temperature. At high temperature (40˚C), the stomatal conductance of greenhouse- and growth chamber-grown leaves is three and four times higher than that measured at lower temperature (25ºC), respectively. The segregation of stom-atal conductance observed in an F2 population obtained from a cross between a primitive cotton (B368) and a modern Pima line (Pima S-6) increased substantially with temperature in both light and darkness. Furthermore, F2 segregants with high stomatal conductance at high temperature were more sensitive to temperature, showing larger changes in conductance in response to an increase in temperature when compared to F2 segregants having low stomatal conductance. Rates of guard cell respiration measured in enzymatically-cleaned epidermal peels, mechanically isolated from the same F2 plants, showed the same temperature dependence. The temperature-induced respiration enhancement was higher in guard cells with high respiration rates. There were positive correlations between stomatal conductance and guard cell respiration rates, and between stomatal conductance and the sensitivity of respiration to changes in temperature. These results imply that guard cell respiration and stomatal conductance co-segregate in Pima cotton plants, suggesting that guard cell respiration is a component of the sensory transduction pathway controlling stomatal responses to temperature.

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Pelicano, Hélène, Rui-hua Xu, Min Du, Li Feng, Ryohei Sasaki, Jennifer S. Carew, Yumin Hu, et al. "Mitochondrial respiration defects in cancer cells cause activation of Akt survival pathway through a redox-mediated mechanism." Journal of Cell Biology 175, no. 6 (December 11, 2006): 913–23. http://dx.doi.org/10.1083/jcb.200512100.

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Cancer cells exhibit increased glycolysis for ATP production due, in part, to respiration injury (the Warburg effect). Because ATP generation through glycolysis is less efficient than through mitochondrial respiration, how cancer cells with this metabolic disadvantage can survive the competition with other cells and eventually develop drug resistance is a long-standing paradox. We report that mitochondrial respiration defects lead to activation of the Akt survival pathway through a novel mechanism mediated by NADH. Respiration-deficient cells (ρ-) harboring mitochondrial DNA deletion exhibit dependency on glycolysis, increased NADH, and activation of Akt, leading to drug resistance and survival advantage in hypoxia. Similarly, chemical inhibition of mitochondrial respiration and hypoxia also activates Akt. The increase in NADH caused by respiratory deficiency inactivates PTEN through a redox modification mechanism, leading to Akt activation. These findings provide a novel mechanistic insight into the Warburg effect and explain how metabolic alteration in cancer cells may gain a survival advantage and withstand therapeutic agents.

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Ryan, Michael G. "Growth and maintenance respiration in stems of Pinuscontorta and Piceaengelmannii." Canadian Journal of Forest Research 20, no. 1 (January 1, 1990): 48–57. http://dx.doi.org/10.1139/x90-008.

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Stem maintenance respiration was linearly related to live-cell volume for lodgepole pine (Pinuscontorta var. latifolia Engelm.) from 4 to 36 cm dbh and for Engelmann spruce (Piceaengelmannii Parry) from 0 to 20 cm dbh. Sapwood contained greater than 80% of the total live-cell volume in stems. Bole surface area, commonly used to estimate tree respiration costs, poorly estimated stem maintenance respiration. At 15 °C, maintenance costs for lodgepole pine were 6.6 × 10−5 kg C•(kg C sapwood)−1•d−1. Stem respiration during the growing season, both corrected and uncorrected for maintenance, correlated well with annual stemwood growth. Annual stem maintenance respiration for trees and stands can be estimated using sapwood volume, sapwood temperature, and knowledge of respiratory behavior. Total respiration (construction plus maintenance) estimated using stem growth and a model of maintenance respiration was compared with actual respiration measurements integrated over a 100-d growing season. Estimated respiration agreed with the integrated measurements for Engelmann spruce, but overestimated the integrated measurements by 73% in lodgepole pine. These results suggest that estimates of stem respiration made during the growing season may be affected by transpiration.

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VanHook, Annalisa M. "Mitochondrial respiration not required." Science Signaling 12, no. 585 (June 11, 2019): eaay2985. http://dx.doi.org/10.1126/scisignal.aay2985.

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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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Pelicano, Hélène, Li Feng, Yan Zhou, Jennifer S. Carew, Elizabeth O. Hileman, William Plunkett, Michael J. Keating, and Peng Huang. "Inhibition of Mitochondrial Respiration." Journal of Biological Chemistry 278, no. 39 (July 9, 2003): 37832–39. http://dx.doi.org/10.1074/jbc.m301546200.

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Matias, Pedro M., Ana V. Coelho, Filipa M. A. Valente, Diana Plácido, Jean LeGall, António V. Xavier, Inês A. C. Pereira, and Maria Arménia Carrondo. "Sulfate Respiration inDesulfovibrio vulgarisHildenborough." Journal of Biological Chemistry 277, no. 49 (September 27, 2002): 47907–16. http://dx.doi.org/10.1074/jbc.m207465200.

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Patro, Edward T. "Teaching Aerobic Cell Respiration Using the 5 Es." American Biology Teacher 70, no. 2 (February 2008): 85–87. http://dx.doi.org/10.1662/0002-7685(2008)70[85:tacrut]2.0.co;2.

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Patro, Edward T. "Teaching Aerobic Cell Respiration Using the 5 Es." American Biology Teacher 70, no. 2 (February 1, 2008): 85–87. http://dx.doi.org/10.2307/30163209.

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Dolenc, D., M. Šentjurc, and G. Serša. "EPR oximetry: Reduction of cell respiration by vinblastine." Pflügers Archiv European Journal of Physiology 431, S6 (November 1996): R261—R262. http://dx.doi.org/10.1007/bf02346368.

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27

Swerdlow, Russell H., Lezi E., Daniel Aires, and Jianghua Lu. "Glycolysis–respiration relationships in a neuroblastoma cell line." Biochimica et Biophysica Acta (BBA) - General Subjects 1830, no. 4 (April 2013): 2891–98. http://dx.doi.org/10.1016/j.bbagen.2013.01.002.

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Riedel, K., P. Liebs, and R. Renneberg. "An electrochemical method for determination of cell respiration." Journal of Basic Microbiology 25, no. 1 (1985): 51–56. http://dx.doi.org/10.1002/jobm.3620250115.

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Mohell, N., E. Connolly, and J. Nedergaard. "Distinction between mechanisms underlying alpha 1- and beta-adrenergic respiratory stimulation in brown fat cells." American Journal of Physiology-Cell Physiology 253, no. 2 (August 1, 1987): C301—C308. http://dx.doi.org/10.1152/ajpcell.1987.253.2.c301.

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Experimental conditions are described for selective alpha 1- and beta-adrenergic stimulation of the respiration of brown fat cells. The dual agonist norepinephrine was unsuitable as a selective alpha 1-agonist, since unacceptably high concentrations of propranolol were needed to abolish the beta-response. Phenylephrine at 50 microM, in the presence of 5 microM dl-propranolol, was shown to lead to a maximal, selective alpha 1-stimulation, whereas maximal, selective beta-stimulation was achieved with 1 microM isoproterenol in the presence of 5 microM prazosin. The mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) was able to further increase respiration that was already maximally alpha 1-stimulated, but when added before the alpha 1-stimulation, FCCP totally abolished the response. In contrast, FCCP had no effect on the beta-stimulated response. Similarly, oligomycin (an inhibitor of mitochondrial ATP synthesis) inhibited alpha 1-respiration but had a much smaller effect on beta-respiration. Ouabain (an inhibitor of the Na+-K+-ATPase) halved alpha 1-respiration but only induced a small inhibition of beta-respiration. It is concluded that only a small fraction of thermogenesis from beta-adrenergic processes is due to oxidative phosphorylation, whereas alpha 1-respiration is largely due to the oxygen cost of mitochondrial ATP synthesis, and a large fraction of this ATP is apparently used for the restoration of ion gradients.

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Esteves, A. Raquel, Jane Lu, Mariana Rodova, Isaac Onyango, E. Lezi, Richard Dubinsky, Kelly E. Lyons, et al. "Mitochondrial respiration and respiration-associated proteins in cell lines created through Parkinson’s subject mitochondrial transfer." Journal of Neurochemistry 113, no. 3 (May 2010): 674–82. http://dx.doi.org/10.1111/j.1471-4159.2010.06631.x.

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Balbina J Plotkin, Ira M Sigar, Amber Kaminski, and Monika I Konaklieva. "Putative pathways fueling anaerobic mitochondrial respiration." World Journal of Advanced Research and Reviews 14, no. 2 (May 30, 2022): 603–12. http://dx.doi.org/10.30574/wjarr.2022.14.2.0464.

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Tumor interiors undergo prolonged anoxia; however, the pathways involved have not been identified. Since NO and H2S function in prokaryotic anaerobic respiration, the effect their pathway elements have on HeLa 229 cell viability was measured after 10 days anaerobic incubation. Arginine or xanthine (NO pathway precursors) increased cell viability (13.1- and 4.4-fold, respectively). The H2S pathway precursor, cysteine, also enhanced viability (9.8-fold), as did H2S donor GYY4137, or inhibitor of glutathione synthesis, propargylglycine, (40- and 85-fold, respectively). These results demonstrate that cell viability after extended anaerobic incubation (10 days) can be modulated by affecting NO or H2S pathways.

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Nag, Maitreyi, and Namita Nandi. "Antidepressants and brain respiration." Bioscience Reports 11, no. 1 (February 1, 1991): 11–14. http://dx.doi.org/10.1007/bf01118600.

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Imipramine and clorgyline, at concentrations of 0.002 M, inhibit the respiration of brain tissue by 82 and 71 per cent respectively, while chloropromazine and tranylcypromine, at concentrations of 0.01 M, inhibit it about 25 per cent. Deprenyl and amphetamine at a concentration of 0.002 M inhibit brain tissue respiration by 12 and 18 per cent respectively. Respiration in brain is least affected by lithium chloride (only 5 per cent inhibition).

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Shafiei, Rasoul, Frank Delvigne, and Phillipe Thonart. "Flow-cytometric assessment of damages to Acetobacter senegalensis during freeze-drying process and storage." Acetic Acid Bacteria 2, no. 1s (February 26, 2013): 10. http://dx.doi.org/10.4081/aab.2013.s1.e10.

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Downstream processes have great influences on bacterial starter production. Different modifications occur to cellular compounds during freeze-drying process and storage of bacterial starters. Consequently, viability and culturability (multiplication capacity) undergo some changes. In this study, the effects of freeze-drying process and storage conditions were examined on cell envelope integrity, respiration and culturability of <em>Acetobacter senegalensis</em>. Freezing of cells protected with mannitol (20% w/w) did not affect cell multiplication and respiration considerably; however, 19% of cells showed compromised cell envelope after freezing. After drying, 1.96×10<sup>11</sup> CFU/g were enumerated, indicating that about 34% of the cells could survive and keep their culturability. Drying of the cells induced further leakage in cell envelope and finally 81% of cells appeared as injured ones; however, 87% of the dried cells maintained their respiration capacity. Storage temperature had significant effect on cell multiplication ability; higher storage temperature (35°C) caused 8.59-log reduction in cell culturability after nine-month period of storage. Collapse of cell envelop integrity and respiration was observed at 35°C. At lower storage temperature (4°C), the culturability decreased about one-log reduction after nine months. Cell envelope integrity was subjected to minor changes during a period of nine month-storage at 4°C whereas a heterogeneous population of cells with different respiration capacity emerged at 4°C. These results indicate that a major part of cells undergone drying process and storage entered into viable but non-culturable state. In addition, usage of different culture media didn’t improve resuscitation. Besides, it seems that sub-lethal damages to cell envelope caused uptake of propidium iodide, however these kinds of injuries could not impress cell multiplications and respiration.

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Brown, Guy C. "Nitric oxide and mitochondrial respiration." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1411, no. 2-3 (May 1999): 351–69. http://dx.doi.org/10.1016/s0005-2728(99)00025-0.

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Tripodi, Farida, Andrea Castoldi, Raffaele Nicastro, Veronica Reghellin, Linda Lombardi, Cristina Airoldi, Ermelinda Falletta, et al. "Methionine supplementation stimulates mitochondrial respiration." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1865, no. 12 (December 2018): 1901–13. http://dx.doi.org/10.1016/j.bbamcr.2018.09.007.

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Bu, Pengli, Shreya Nagar, Madhura Bhagwat, Pritpal Kaur, Ankita Shah, Joey Zeng, Ivana Vancurova, and Ales Vancura. "DNA damage response activates respiration and thereby enlarges dNTP pools to promote cell survival in budding yeast." Journal of Biological Chemistry 294, no. 25 (May 9, 2019): 9771–86. http://dx.doi.org/10.1074/jbc.ra118.007266.

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The DNA damage response (DDR) is an evolutionarily conserved process essential for cell survival. Previously, we found that decreased histone expression induces mitochondrial respiration, raising the question whether the DDR also stimulates respiration. Here, using oxygen consumption and ATP assays, RT-qPCR and ChIP-qPCR methods, and dNTP analyses, we show that DDR activation in the budding yeast Saccharomyces cerevisiae, either by genetic manipulation or by growth in the presence of genotoxic chemicals, induces respiration. We observed that this induction is conferred by reduced transcription of histone genes and globally decreased DNA nucleosome occupancy. This globally altered chromatin structure increased the expression of genes encoding enzymes of tricarboxylic acid cycle, electron transport chain, oxidative phosphorylation, elevated oxygen consumption, and ATP synthesis. The elevated ATP levels resulting from DDR-stimulated respiration drove enlargement of dNTP pools; cells with a defect in respiration failed to increase dNTP synthesis and exhibited reduced fitness in the presence of DNA damage. Together, our results reveal an unexpected connection between respiration and the DDR and indicate that the benefit of increased dNTP synthesis in the face of DNA damage outweighs possible cellular damage due to increased oxygen metabolism.

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Merce, Adrian P., Anca M. Bînă, Vlad F. Avram, Darius G. Buriman, Ana Lascu, Horea B. Feier, Lucian Petrescu, Danina M. Muntean, Eskil Elmér, and Octavian M. Crețu. "Cell-Permeable Succinate Improves Platelet Respiration in Patients Undergoing Cardiopulmonary Bypass: A Pilot Study." Timisoara Medical Journal 2022, no. 2 (August 16, 2022): 1. http://dx.doi.org/10.35995/tmj20220202.

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Open-heart surgery with cardiopulmonary bypass (CPB) remains the standard approach for complex cardiac pathologies, such as advanced coronary heart disease and severe valvular defects. Platelet dysfunction has been widely reported, with both structural and functional changes being elicited by the CPB circuit. Succinate is a mitochondrial substrate that is metabolized through complex II (CII) but is impermeable to cellular membranes when given exogenously. Cell-permeable succinates are novel prodrugs developed to support mitochondrial electron transport (ET) and prevent energy depletion in various pathologies. The aim of the present pilot study was to investigate the role of NV118 (diacetoxymethyl succinate), a cell-permeable succinate, on platelet respiration in a pilot group of patients undergoing CPB. Blood samples (20 mL) were collected from participants before (prior to heparin administration) and after CPB (within 10 min after protamine sulphate administration). Platelets were isolated through a two-step centrifugation protocol. Mitochondrial respiration was analyzed by means of high-resolution respirometry in the presence of NV118 or its solvent (DMSO). The main respiratory parameters recorded were as follows: ROUTINE respiration, LEAK respiration, and maximal uncoupled respiration for both CI and CII (ET capacity) and for CII solely after CI inhibition (ET CII capacity). Here, we report that NV118 elicited a global increase in platelet respiration both pre- and post-CPB. In conclusion, NV118, a cell-permeable succinate, improved platelet bioenergetics in the setting of cardiopulmonary bypass. Whether the compound can support platelet function and/or provide organ protection at the mitochondrial level during CPB are clearly worthy and important areas for future investigation.

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Darenova, Eva, Petr Horáček, Jan Krejza, Radek Pokorný, and Marian Pavelka. "Seasonally varying relationship between stem respiration, increment and carbon allocation of Norway spruce trees." Tree Physiology 40, no. 7 (April 9, 2020): 943–55. http://dx.doi.org/10.1093/treephys/tpaa039.

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Abstract Stem respiration is an important component of an ecosystem’s carbon budget. Beside environmental factors, it depends highly on tree energy demands for stem growth. Determination of the relationship between stem growth and stem respiration would help to reveal the response of stem respiration to changing climate, which is expected to substantially affect tree growth. Common measurement of stem radial increment does not record all aspects of stem growth processes, especially those connected with cell wall thickening; therefore, the relationship between stem respiration and stem radial increment may vary depending on the wood cell growth differentiation phase. This study presents results from measurements of stem respiration and increment carried out for seven growing seasons in a young Norway spruce forest. Moreover, rates of carbon allocation to stems were modeled for these years. Stem respiration was divided into maintenance (Rm) and growth respiration (Rg) based upon the mature tissue method. There was a close relationship between Rg and daily stem radial increment (dSRI), and this relationship differed before and after dSRI seasonal maximum, which was around 19 June. Before this date, Rg increased exponentially with dSRI, while after this date logarithmically. This is a result of later maxima of Rg and its slower decrease when compared with dSRI, which is connected with energy demands for cell wall thickening. Rg reached a maxima at the end of June or in July. The maximum of carbon allocation to stem peaked in late summer, when Rg mostly tended to decrease. The overall contribution of Rg to stem CO2 efflux amounted to 46.9% for the growing period from May to September and 38.2% for the year as a whole. This study shows that further deeper analysis of in situ stem growth and stem respiration dynamics is greatly needed, especially with a focus on wood formation on a cell level.

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39

Europe Finner, G. N., H. S. Tillinghast, S. J. McRobbie, and P. C. Newell. "TMB-8 inhibits respiration and cyclic GMP formation in Dictyostelium discoideum." Journal of Cell Science 79, no. 1 (November 1, 1985): 151–60. http://dx.doi.org/10.1242/jcs.79.1.151.

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The putative inhibitor of intracellular calcium mobilization, TMB-8 was found to be a powerful inhibitor of respiration in amoebae of Dictyostelium discoideum. Consequently, the previously reported effects of this drug on cyclic GMP formation induced by chemoattractants were reassessed. It was found that TMB-8 abolished both folate and cyclic AMP-mediated accumulation of cyclic GMP in D. discoideum amoebae and that addition of Ca2+ completely restored this response. The Ca2+ chelating agent EGTA did not mimic the effect of TMB-8. The effect on cyclic GMP formation, however, occurred only at a concentration of TMB-8 that was ten times that causing maximal inhibition of respiration, and inhibition of cyclic GMP formation was completely restored by addition of excess Ca2+, whereas inhibition of respiration was only partially restored. The data suggest that TMB-8 has more than one inhibitory action, and because of the differential sensitivity of respiration and cyclic GMP formation to this drug, and the differential antagonism of excess Ca2+, we conclude that the effect of TMB-8 on the cyclic GMP response is probably due to its effect on Ca2+ mobilization, rather than indirectly via its effects on respiration. However, we advise caution in interpretation of data using this inhibitor where the responses measured are prolonged, are energy-requiring or are not freely reversible by excess Ca2+.

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40

Ray, S., S. Dutta, J. Halder, and M. Ray. "Inhibition of electron flow through complex I of the mitochondrial respiratory chain of Ehrlich ascites carcinoma cells by methylglyoxal." Biochemical Journal 303, no. 1 (October 1, 1994): 69–72. http://dx.doi.org/10.1042/bj3030069.

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The effect of methylglyoxal on the oxygen consumption of Ehrlich-ascites-carcinoma (EAC)-cell mitochondria was tested by using different respiratory substrates, electron donors at different segments of the mitochondrial respiratory chain and site-specific inhibitors to identify the specific respiratory complex which might be involved in the inhibitory effect of methylglyoxal on the oxygen consumption by these cells. The results indicate that methylglyoxal strongly inhibits ADP-stimulated alpha-oxo-glutarate and malate plus pyruvate-dependent respiration, whereas, at a much higher concentration, methylglyoxal fails to inhibit succinate-dependent respiration. Methylglyoxal also fails to inhibit respiration which is initiated by duroquinol, an artificial electron donor. Moreover, methylglyoxal cannot inhibit oxygen consumption when the NNN'N′-tetramethyl-p-phenylenediamine by-pass is used. The inhibitory effect of methylglyoxal is identical on both ADP-stimulated and uncoupler-stimulated respiration. Lactaldehyde, a catabolite of methylglyoxal, can exert a protective effect on the inhibition of EAC-cell mitochondrial respiration by methylglyoxal. We suggest that methylglyoxal possibly inhibits the electron flow through complex I of the EAC-cell mitochondrial respiratory chain.

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41

CIVELEK, Vildan N., Jude T. DEENEY, Nicholas J. SHALOSKY, Keith TORNHEIM, Richard G. HANSFORD, Marc PRENTKI, and Barbara E. CORKEY. "Regulation of pancreatic β-cell mitochondrial metabolism: influence of Ca2+, substrate and ADP." Biochemical Journal 318, no. 2 (September 1, 1996): 615–21. http://dx.doi.org/10.1042/bj3180615.

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To gain insight into the regulation of pancreatic β-cell mitochondrial metabolism, the direct effects on respiration of different mitochondrial substrates, variations in the ATP/ADP ratio and free Ca2+ were examined using isolated mitochondria and permeabilized clonal pancreatic β-cells (HIT). Respiration from pyruvate was high and not influenced by Ca2+ in State 3 or under various redox states and fixed values of the ATP/ADP ratio; nevertheless, high Ca2+ elevated pyridine nucleotide fluorescence, indicating activation of pyruvate dehydrogenase by Ca2+. Furthermore, in the presence of pyruvate, elevated Ca2+ stimulated CO2 production from pyruvate, increased citrate production and efflux from the mitochondria and inhibited CO2 production from palmitate. The latter observation suggests that β-cell fatty acid oxidation is not regulated exclusively by malonyl-CoA but also by the mitochondrial redox state. α-Glycerophosphate (α-GP) oxidation was Ca2+-dependent with a half-maximal rate observed at around 300 nM Ca2+. We have recently demonstrated that increases in respiration precede increases in Ca2+ in glucose-stimulated clonal pancreatic β-cells (HIT), indicating that Ca2+ is not responsible for the initial stimulation of respiration [Civelek, Deeney, Kubik, Schultz, Tornheim and Corkey (1996) Biochem. J. 315, 1015–1019]. It is suggested that respiration is stimulated by increased substrate (α-GP and pyruvate) supply together with oscillatory increases in ADP [Nilsson, Schultz, Berggren, Corkey and Tornheim (1996) Biochem. J. 314, 91–94]. The rise in Ca2+, which in itself may not significantly increase net respiration, could have the important functions of (1) activating the α-GP shuttle, to maintain an oxidized cytosol and high glycolytic flux; (2) activating pyruvate dehydrogenase, and indirectly pyruvate carboxylase, to sustain production of citrate and hence the putative signal coupling factors, malonyl-CoA and acyl-CoA; and (3) increasing mitochondrial redox state to implement the switch from fatty acid to pyruvate oxidation.

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Beltran, B., B. K. Kemp, and S. Moncada. "Nitric oxide on cell respiration: Its role in cell survival or death." Journal of Molecular and Cellular Cardiology 33, no. 6 (June 2001): A156. http://dx.doi.org/10.1016/s0022-2828(01)90601-7.

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43

Masci, Alessandra, Daniela Mastronicola, Marzia Arese, Maria Piane, Andrea De Amicis, Thomas J. J. Blanck, Luciana Chessa, and Paolo Sarti. "Control of cell respiration by nitric oxide in Ataxia Telangiectasia lymphoblastoid cells." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1777, no. 1 (January 2008): 66–73. http://dx.doi.org/10.1016/j.bbabio.2007.10.016.

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Costa, L. E., G. Mendez, and A. Boveris. "Oxygen dependence of mitochondrial function measured by high-resolution respirometry in long-term hypoxic rats." American Journal of Physiology-Cell Physiology 273, no. 3 (September 1, 1997): C852—C858. http://dx.doi.org/10.1152/ajpcell.1997.273.3.c852.

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Respiration and oxidative phosphorylation were investigated in tightly coupled mitochondria isolated from liver and heart of rats submitted to a simulated altitude of 4,400 m for 14-15 mo and their corresponding controls at sea level. High-resolution respirometry was utilized to determine the apparent Michaelis-Menten constant for ADP and O2 (K(m)-ADP and K(m)-O2, respectively), the latter under active and resting states of mitochondrial respiration. The K(m)-O2 in mitochondria isolated from normoxic rats was higher for active (state 3) than for resting (state 4) respiration; the values decreased from 1.5 and 1.7 to 0.25 and 0.30 microM in heart and liver mitochondria, respectively. The K(m)-O2 values found in the active state suggest a role for the normally occurring intracellular PO2 range reported in the literature in the regulation of cellular respiration. No changes were found in the ADP or O2 dependence of respiration in the mitochondria isolated from long-term acclimatized rats compared with their controls, indicating that the intrinsic properties and the efficiency of mitochondria do not change as a consequence of adaptation to hypoxia.

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45

Cruz, Pablo, Ulises Ahumada-Castro, Galdo Bustos, Jordi Molgó, Daniela Sauma, Alenka Lovy, and César Cárdenas. "Inhibition of InsP3R with Xestospongin B Reduces Mitochondrial Respiration and Induces Selective Cell Death in T Cell Acute Lymphoblastic Leukemia Cells." International Journal of Molecular Sciences 22, no. 2 (January 11, 2021): 651. http://dx.doi.org/10.3390/ijms22020651.

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy whose chemoresistance and relapse persist as a problem despite significant advances in its chemotherapeutic treatments. Mitochondrial metabolism has emerged as an interesting therapeutic target given its essential role in maintaining bioenergetic and metabolic homeostasis. T-ALL cells are characterized by high levels of mitochondrial respiration, making them suitable for this type of intervention. Mitochondrial function is sustained by a constitutive transfer of calcium from the endoplasmic reticulum to mitochondria through the inositol 1,4,5-trisphosphate receptor (InsP3R), making T-ALL cells vulnerable to its inhibition. Here, we determine the bioenergetic profile of the T-ALL cell lines CCRF-CEM and Jurkat and evaluate their sensitivity to InsP3R inhibition with the specific inhibitor, Xestospongin B (XeB). Our results show that T-ALL cell lines exhibit higher mitochondrial respiration than non-malignant cells, which is blunted by the inhibition of the InsP3R. Prolonged treatment with XeB causes T-ALL cell death without affecting the normal counterpart. Moreover, the combination of XeB and glucocorticoids significantly enhanced cell death in the CCRF-CEM cells. The inhibition of InsP3R with XeB rises as a potential therapeutic alternative for the treatment of T-ALL.

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46

Cruz, Pablo, Ulises Ahumada-Castro, Galdo Bustos, Jordi Molgó, Daniela Sauma, Alenka Lovy, and César Cárdenas. "Inhibition of InsP3R with Xestospongin B Reduces Mitochondrial Respiration and Induces Selective Cell Death in T Cell Acute Lymphoblastic Leukemia Cells." International Journal of Molecular Sciences 22, no. 2 (January 11, 2021): 651. http://dx.doi.org/10.3390/ijms22020651.

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy whose chemoresistance and relapse persist as a problem despite significant advances in its chemotherapeutic treatments. Mitochondrial metabolism has emerged as an interesting therapeutic target given its essential role in maintaining bioenergetic and metabolic homeostasis. T-ALL cells are characterized by high levels of mitochondrial respiration, making them suitable for this type of intervention. Mitochondrial function is sustained by a constitutive transfer of calcium from the endoplasmic reticulum to mitochondria through the inositol 1,4,5-trisphosphate receptor (InsP3R), making T-ALL cells vulnerable to its inhibition. Here, we determine the bioenergetic profile of the T-ALL cell lines CCRF-CEM and Jurkat and evaluate their sensitivity to InsP3R inhibition with the specific inhibitor, Xestospongin B (XeB). Our results show that T-ALL cell lines exhibit higher mitochondrial respiration than non-malignant cells, which is blunted by the inhibition of the InsP3R. Prolonged treatment with XeB causes T-ALL cell death without affecting the normal counterpart. Moreover, the combination of XeB and glucocorticoids significantly enhanced cell death in the CCRF-CEM cells. The inhibition of InsP3R with XeB rises as a potential therapeutic alternative for the treatment of T-ALL.

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47

Avram, Vlad Florian, Anca Mihaela Bîna, Alexandra Sima, Oana Maria Aburel, Adrian Sturza, Ovidiu Burlacu, Romulus Zorin Timar, Danina Mirela Muntean, Eskil Elmér, and Octavian Marius Crețu. "Improvement of Platelet Respiration by Cell–Permeable Succinate in Diabetic Patients Treated with Statins." Life 11, no. 4 (March 28, 2021): 288. http://dx.doi.org/10.3390/life11040288.

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Diabetes mellitus (DM) is the most severe metabolic disease that reached the level of a global pandemic and is associated with high cardiovascular morbidity. Statins are the first–line lipid–lowering therapy in diabetic patients with or without a history of atherosclerotic disease. Although well tolerated, chronic treatment may result in side effects that lead to treatment interruption. Mitochondrial dysfunction has emerged as a central pathomechanism in DM– and statin–induced side effects. Assessment of mitochondrial respiration in peripheral platelets has been increasingly used as a mirror of organ mitochondrial dysfunction. The present study aimed to assess the: (i) changes in mitochondrial respiration elicited by statins in patients with type 2 DM and (ii) the effects of cell–permeable succinate (NV118) on respiratory parameters in platelets harvested from these patients. No significant changes were found in global mitochondrial respiration of intact platelets isolated from diabetic patients treated with either atorvastatin or rosuvastatin. Similarly, no significant changes in mitochondrial respiration of permeabilized platelets were found between diabetic patients treated with atorvastatin and healthy controls. Acute ex vivo administration of NV118 significantly improved respiration in isolated platelets. These results prompt further research on the role of permeable succinate as a therapeutic alternative for improving mitochondrial function in metabolic pathologies and point to the role of peripheral platelets as a potential biomarker of treatment response.

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Komarkova, Eliska, Jan Paca, Eva Klapkova, Marie Stiborova, Carlos R. Soccol, and Miroslav Sobotka. "Physiological changes of Candida tropicalis population degrading phenol in fed batch reactor." Brazilian Archives of Biology and Technology 46, no. 4 (December 2003): 537–43. http://dx.doi.org/10.1590/s1516-89132003000400007.

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Candida tropicalis can use phenol as the sole carbon and energy source. Experiments regarding phenol degradations from the water phase were carried out. The fermentor was operated as a fed-batch system with oxistat control. Under conditions of nutrient limitation and an excess of oxygen the respiration activity of cells was suppressed and some color metabolites (black-brown) started to be formed. An accumulation of these products inhibited the cell growth under aerobic conditions. Another impact was a decrease of the phenol hydroxylase activity as the key enzyme of the phenol degradation pathway at the end of the cell respiration activity. This decrease is linked with the above mentioned product inhibition. The cell death studied by fluorescent probe proceeded very slowly after the loss of the respiration activity. The starvation stress induced an increase of the endogenous respiration rate at the expense of phenol oxidation.

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Baeder, Andrea C., Kiran Napa, Sarah T. Richardson, Oliver J. Taylor, Samantha G. Andersen, Shalene H. Wilcox, Duane R. Winden, Paul R. Reynolds, and Benjamin T. Bikman. "Oral Gingival Cell Cigarette Smoke Exposure Induces Muscle Cell Metabolic Disruption." International Journal of Dentistry 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/2763160.

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Cigarette smoke exposure compromises health through damaging multiple physiological systems, including disrupting metabolic function. The purpose of this study was to determine the role of oral gingiva in mediating the deleterious metabolic effects of cigarette smoke exposure on skeletal muscle metabolic function. Using an in vitro conditioned medium cell model, skeletal muscle cells were incubated with medium from gingival cells treated with normal medium or medium containing suspended cigarette smoke extract (CSE). Following incubation of muscle cells with gingival cell conditioned medium, muscle cell mitochondrial respiration and insulin signaling and action were determined as an indication of overall muscle metabolic health. Skeletal muscle cells incubated with conditioned medium of CSE-treated gingival cells had a profound reduction in mitochondrial respiration and respiratory control. Furthermore, skeletal muscle cells had a greatly reduced response in insulin-stimulated Akt phosphorylation and glycogen synthesis. Altogether, these results provide a novel perspective on the mechanism whereby cigarette smoke affects systemic metabolic function. In conclusion, we found that oral gingival cells treated with CSE create an altered milieu that is sufficient to both disrupted skeletal muscle cell mitochondrial function and insulin sensitivity.

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Agarwal, Amit R., Fei Yin, and Enrique Cadenas. "Metabolic shift in lung alveolar cell mitochondria following acrolein exposure." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 10 (November 15, 2013): L764—L773. http://dx.doi.org/10.1152/ajplung.00165.2013.

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Acrolein, an α,β unsaturated electrophile, is an environmental pollutant released in ambient air from diesel exhausts and cooking oils. This study examines the role of acrolein in altering mitochondrial function and metabolism in lung-specific cells. RLE-6TN, H441, and primary alveolar type II (pAT2) cells were exposed to acrolein for 4 h, and its effect on mitochondrial oxygen consumption rates was studied by XF Extracellular Flux analysis. Low-dose acrolein exposure decreased mitochondrial respiration in a dose-dependent manner because of alteration in the metabolism of glucose in all the three cell types. Acrolein inhibited glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity, leading to decreased substrate availability for mitochondrial respiration in RLE-6TN, H441, and pAT2 cells; the reduced GAPDH activity was compensated in pAT2 cells by an increase in the activity of glucose-6-phosphate dehydrogenase, the regulatory control of the pentose phosphate pathway. The decrease in pyruvate from glucose metabolism resulted in utilization of alternative sources to support mitochondrial energy production: palmitate-BSA complex increased mitochondrial respiration in RLE-6TN and pAT2 cells. The presence of palmitate in alveolar cells for surfactant biosynthesis may prove to be the alternative fuel source for mitochondrial respiration. Accordingly, a decrease in phosphatidylcholine levels and an increase in phospholipase A2 activity were found in the alveolar cells after acrolein exposure. These findings have implications for understanding the decrease in surfactant levels frequently observed in pathophysiological situations with altered lung function following exposure to environmental toxicants.

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Journal articles on the topic 'Cell respiration'

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