scholarly journals Teaching Aerobic Cell Respiration Using the 5 Es

2008 ◽  
Vol 70 (2) ◽  
pp. 85-87
Author(s):  
Edward T. Patro
Keyword(s):  
Cell Respiration ◽  
Aerobic Cell

scholarly journals Ketogenic diets inhibit mitochondrial biogenesis and induce cardiac fibrosis

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Sha Xu ◽  
Hui Tao ◽  
Wei Cao ◽  
Li Cao ◽  
Yan Lin ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
Ketone Body ◽  
Cardiac Fibrosis ◽  
Cardiomyocyte Apoptosis ◽  
Healthy Individuals ◽  
Cell Respiration ◽  
Ketogenic Diets ◽  
Mitochondrial Ribosome ◽  
Encoding Genes ◽  
Human Atrial Fibrillation

AbstractIn addition to their use in relieving the symptoms of various diseases, ketogenic diets (KDs) have also been adopted by healthy individuals to prevent being overweight. Herein, we reported that prolonged KD exposure induced cardiac fibrosis. In rats, KD or frequent deep fasting decreased mitochondrial biogenesis, reduced cell respiration, and increased cardiomyocyte apoptosis and cardiac fibrosis. Mechanistically, increased levels of the ketone body β-hydroxybutyrate (β-OHB), an HDAC2 inhibitor, promoted histone acetylation of the Sirt7 promoter and activated Sirt7 transcription. This in turn inhibited the transcription of mitochondrial ribosome-encoding genes and mitochondrial biogenesis, leading to cardiomyocyte apoptosis and cardiac fibrosis. Exogenous β-OHB administration mimicked the effects of a KD in rats. Notably, increased β-OHB levels and SIRT7 expression, decreased mitochondrial biogenesis, and increased cardiac fibrosis were detected in human atrial fibrillation heart tissues. Our results highlighted the unknown detrimental effects of KDs and provided insights into strategies for preventing cardiac fibrosis in patients for whom KDs are medically necessary.

scholarly journals Leaf proteome modulation and cytological features of seagrass Cymodocea nodosa in response to long-term high CO2 exposure in volcanic vents

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Amalia Piro ◽  
Letizia Bernardo ◽  
Ilia Anna Serra ◽  
Isabel Barrote ◽  
Irene Olivé ◽  
...  
Keyword(s):  
Metabolic Pathways ◽  
Total Protein Content ◽  
Cymodocea Nodosa ◽  
Cell Respiration ◽  
Strong Reduction ◽  
Vulcano Island ◽  
Leaf Tissues ◽  
Cytological Features ◽  
Harvesting Process

AbstractSeagrass Cymodocea nodosa was sampled off the Vulcano island, in the vicinity of a submarine volcanic vent. Leaf samples were collected from plants growing in a naturally acidified site, influenced by the long-term exposure to high CO2 emissions, and compared with others collected in a nearby meadow living at normal pCO2 conditions. The differential accumulated proteins in leaves growing in the two contrasting pCO2 environments was investigated. Acidified leaf tissues had less total protein content and the semi-quantitative proteomic comparison revealed a strong general depletion of proteins belonging to the carbon metabolism and protein metabolism. A very large accumulation of proteins related to the cell respiration and to light harvesting process was found in acidified leaves in comparison with those growing in the normal pCO2 site. The metabolic pathways linked to cytoskeleton turnover also seemed affected by the acidified condition, since a strong reduction in the concentration of cytoskeleton structural proteins was found in comparison with the normal pCO2 leaves. Results coming from the comparative proteomics were validated by the histological and cytological measurements, suggesting that the long lasting exposure and acclimation of C. nodosa to the vents involved phenotypic adjustments that can offer physiological and structural tools to survive the suboptimal conditions at the vents vicinity.

scholarly journals CELL RESPIRATION STUDIES

1927 ◽  
Vol 46 (1) ◽  
pp. 43-51
Author(s):  
Blake C. Wilbur ◽  
Geneva A. Daland ◽  
John Cohen
Keyword(s):  
Oxygen Consumption ◽  
Whole Blood ◽  
Repeated Measurements ◽  
Closed Space ◽  
Cell Respiration ◽  
Chemical Substances ◽  
Normal Individuals ◽  
Tissue Cells

A description is given of a closed space respiration apparatus which can be used to determine the amount of gas used or liberated by living blood or tissue cells, or chemical substances. Continuous observations can be made and repeated measurements recorded without interrupting the vital processes or destroying the cells. Studies of the oxygen consumption by whole blood in normal individuals and in patients with leucocytosis and myelogenous leucemia, as well as by white cells suspended in plasma, will be reported in subsequent papers.

scholarly journals A manometric analysis of the metabolism in avian ontogenesis―II. The effects of fluoride, Iodoacetate, and other reagents on the respiration of blastoderm, embryo, and yolk-sac

1932 ◽  
Vol 112 (775) ◽  
pp. 114-138 ◽  
Keyword(s):  
Intact Cell ◽  
Good Deal ◽  
Iodoacetic Acid ◽  
Embryonic Cells ◽  
Secondary Effects ◽  
Cell Respiration ◽  
Cell Interior ◽  
Cellular Mechanisms ◽  
Differential Attack ◽  
Biological Methods

The study of cell-respiration by means of agents with a known action upon some one part of the cellular mechanisms has in recent years been much pursued, and it has to some extent been possible to make a differential attack upon the various co-operating processes which are so efficiently integrated in the intact cell. These methods suffer, it is true, from the disadvantage that the addition of an ion such as fluoride to the cell-interior may not merely inhibit a certain reaction which normally goes on there, but may also bring into being a number of distinctively pathological reactions which have no place in the normal cell. It is not surprising, therefore, that the results of experiments on cell-respiration are difficult to interpret. But difficulties of interpretation are no ground for failing to make use of any methods. which are available, and the possibility of complicated secondary effects is, after all, common to all biological methods in which the normal course of events within the organism is interfered with. Up to the present time, the study of the effect of agents such as fluoride, cyanide, iodoacetic acid, triphenylmethane dyes, sulphides, pyrophosphates, etc., has been confined to the cells of adult tissues ( cf . Dixon, 1929; wurmser, 1930) or to bacteria ( e. g ., Haldane, Cook and Mapson, 1931). But it would obviously be of much interest to observe their effects upon cells of early embryonic stages for we might hope in this way to discover something of the way in which the chemical machinery of the cell is laid down. To what extent, for instance, do the cells of a somite in a two-day old chick embryo resemble adult muscle cells in their reactions to the glycolysis-inhibiting action of iodoacetic acid ? Moreover, a good deal of evidence exists that embryos in the earlier stages of development combust carbohydrate molecules exclusively, and that later on the combustion of protein and fat sets in. What will happen then, to the metabolism of embryonic cells in the carbohydrate stage if their glycolysing power is artificially inhibited? Is the power of deaminating and combusting amino-acids already present and not used, or has it not yet developed ? In the former case the respiratory quotient should betray a change over to protein combustion; in the latter case the cells should cease to respire altogether. It was to answer questions such as these that the work described in the present paper was undertaken.

Mitochondrial calcium overload triggers complement-dependent superoxide-mediated programmed cell death in Trypanosoma cruzi

2009 ◽  
Vol 418 (3) ◽  
pp. 595-604 ◽  
Author(s):  
Florencia Irigoín ◽  
Natalia M. Inada ◽  
Mariana P. Fernandes ◽  
Lucía Piacenza ◽  
Fernanda R. Gadelha ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Trypanosoma Cruzi ◽  
Complement Activation ◽  
Superoxide Radical ◽  
Membrane Attack Complex ◽  
Cell Respiration ◽  
Mitochondrial Uncoupling ◽  
O2 Production ◽  
Complement Deposition

The epimastigote stage of Trypanosoma cruzi undergoes PCD (programmed cell death) when exposed to FHS (fresh human serum). Although it has been known for over 30 years that complement is responsible for FHS-induced death, the link between complement activation and triggering of PCD has not been established. We have previously shown that the mitochondrion participates in the orchestration of PCD in this model. Several changes in mitochondrial function were described, and in particular it was shown that mitochondrion-derived O2•− (superoxide radical) is necessary for PCD. In the present study, we establish mitochondrial Ca2+ overload as the link between complement deposition and the observed changes in mitochondrial physiology and the triggering of PCD. We show that complement activation ends with the assembly of the MAC (membrane attack complex), which allows influx of Ca2+ and release of respiratory substrates to the medium. Direct consequences of these events are accumulation of Ca2+ in the mitochondrion and decrease in cell respiration. Mitochondrial Ca2+ causes partial dissipation of the inner membrane potential and consequent mitochondrial uncoupling. Moreover, we provide evidence that mitochondrial Ca2+ overload is responsible for the increased O2•− production, and that if cytosolic Ca2+ rise is not accompanied by the accumulation of the cation in the mitochondrion and consequent production of O2•−, epimastigotes die by necrosis instead of PCD. Thus our results suggest a model in which MAC assembly on the parasite surface allows Ca2+ entry and its accumulation in the mitochondrion, leading to O2•− production, which in turn constitutes a PCD signal.

scholarly journals Influence of cyclophosphamide on respiration and membrane permeability of plant cells

2014 ◽  
Vol 49 (4) ◽  
pp. 357-361 ◽  
Author(s):  
Maria Podbielkowska ◽  
Alicja Zobel ◽  
Maria Wałęza
Keyword(s):  
Membrane Permeability ◽  
Cell Membranes ◽  
Alkylating Agents ◽  
Plant Cells ◽  
Cellular Respiration ◽  
Cell Respiration ◽  
Experimental Conditions ◽  
Specific Influence

A specific influence of cyclophosphamide, an oncostatic drug of the group of alkylating agents, has been demonstrated on cellular respiration and the permeability of cell membranes. The tested drug under the experimental conditions inhibites cell respiration by about 20-30 per cent as compared with the control. The permeability of the plasmalemma and tonoplast de-creased markedly under the action of cyclophosphamide.

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