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Metabolic Cardiology
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The energy-starved heart is often not considered by physicians who treat cardiac disease on a day-to-day basis. Angiotensin-converting enzyme inhibitors and angiotensin receptor II blockers improve survival in ischemic and non-ischemic HFs and should be considered as a conventional approach in any patient with heart failure. However, therapies that target the cardiomyocyte itself must also be employed as it has been shown that cardiomyocytes in the failing heart, although metabolically compromised, and their function can be potentially improved and restored. Therapies that go beyond symptomatic relief (diuretics), and the neurohormonal axis, must also be considered that target the cellular, mitochondrial and metabolic defects. Metabolic support with D-ribose, CoQ10, L-carnitine and magnesium is critical for the maintenance of contractile reserve and energy charge in minimally oxidative ischemic or hypoxic hearts. Preservation of cellular energy charge provides the chemical driving force required to complete ATPase reactions needed to maintain cell and tissue viability and function. D-ribose, CoQ10, L-carnitine and magnesium exert a physiological benefit that has a positive impact on cardiac function.
Alteration in Cell Cycle Control Factors and the Induction of Oxygen-Regulated Proteins by Hypoxic Stress
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Harold C. Smith, Robert L. Howell, John W. Ludlow
The trivial explanation for this effect, namely, that pRB phosphorylation state in hypoxic cells simply reflects the reduced energy charge of the cells, does not appear to be the complete story. Cyclin A belongs to a family of proteins known as cyclins, the primary function of which appears to be modulation of the activities of specific kinases and cell cycle regulatory factors through a direct interaction.45,47,51,52 Cyclin A and its interactions appear to be important for S phase progression. This protein is rapidly synthesized during S phase and subsequently rapidly degraded as a prerequisite to M phase progression. Cyclin A is targeted for proteolysis through an ATP-dependent phosphorylation.53 If the loss of energy charge in hypoxic cells was strictly responsible for pRB hypophosphorylation, then it would be anticipated that cyclin A could not be degraded. In contrast, the data show that cyclin A is rapidly lost from hypoxic cells and is not resynthesized until the cells are reoxygenated (Figures 3 and 4). These data suggest that hypoxia may impair cell cycle progression by specifically affecting control through key cell cycle regulatory factors. It is also of interest that alterations in the phosphorylation state of pRB and the turnover of cyclin A in hypoxic cells appear to be uncoupled from the requirement that cells overtly progress through the cell cycle in response to these changes.
Studies on Anoxic Depolarization
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Energy charge in SD is not decreased.42 By contrast, neuronal ATP is largely depleted during anoxia.31,34 It is reasonable to hypothesize that such a dramatic decline in neuronal energy stores is the first step in the chain of events that leads to AD.
Reproductive senescence and energetic metabolism of human luteinized granulosa cells: is it all about ATP? A prospective cohort and critical view
Published in Gynecological Endocrinology, 2021
Gustavo N. Cecchino, Alberto Pacheco, Juan A. García-Velasco
Cellular bioenergetics comprises complex biochemical and biophysical processes [33–35]. As proposed by Atkinson et al. [36], the energy charge accounts for AMP, ADP and ATP concentrations, and accurately reflects the energy status of cells. Normally, the turnover time of the intracellular ATP pool is of the order of a few seconds and the energy charge is maintained with a value that comes close to 0.9, despite oscillations in adenine nucleotide concentrations [37]. Studies on metabolic stress have shown that, unless energy stress is severe, cellular ATP levels remain fairly constant. However, a minimal drop in ATP concentration is accompanied by a significant increase in both ADP and AMP levels [33]. As AMP concentration is usually quite low and technically difficult to assess, the ADP/ATP ratio is considered the most relevant parameter to determine the energy status of a living cell [33–35].
Anti-biofilm activity of dodecyltrimethylammonium chloride microcapsules against Salmonella enterica serovar Enteritidis and Staphylococcus aureus
Published in Biofouling, 2021
Simon Khelissa, Adem Gharsallaoui, Jian Wang, Emilie Dumas, Alexandre Barras, Charafeddine Jama, Fouzia Jbilou, Noureddine Loukili, Nour-Eddine Chihib
The current results showed that the authors’ adopted strategy can be applied as a simple and reliable indicator of cytoplasmic membrane damage by QACs and other antibacterial compounds. Moreover, SEM observation demonstrated the damage to the bacterial membrane caused by DTAC treatment. These results are in accordance with results obtained by the release of fluorescence from E. coli. Similar observations were reported in previous studies (Khelissa et al. 2019, 2019a). Like any other QAC, DTAC is toxic to mammalian cells (Ferk et al. 2007; Inácio et al. 2013). Inácio et al. (2013) showed that QAC induced toxicity in mammalian columnar epithelial cell cultures in vitro at very low concentrations. It is believed that at low concentrations, QACs commonly induce apoptosis in mammalian cells by inducing mitochondrial dysfunction (Rogers and Higgins 1973). At higher doses QACs trigger the complete breakdown of cellular energy charge and necrotic cell death (Debbasch et al. 2001; Levine et al. 2007; Perani et al. 2001). The current results showed that the microencapsulation of DTAC significantly reduced (up to 32-fold) its cytotoxicity towards HeLa cells. Thus, spray drying microencapsulation can be used as an effective tool to enhance the antibacterial activity of DTAC while reducing the quantity of this surfactant required.
Effects of tannic acid in streptozotocin-induced sporadic Alzheimer’s Disease: insights into memory, redox status, Na+, K+-ATPase and acetylcholinesterase activity
Published in Archives of Physiology and Biochemistry, 2022
Mariana F. B. Gerzson, Simone M. Pacheco, Mayara S. P. Soares, Natália P. Bona, Pathise S. Oliveira, Juliana H. Azambuja, Pauline da Costa, Jessié M. Gutierres, Fabiano B. Carvalho, Vera M. Morsch, Roselia M. Spanevello, Francieli M. Stefanello
In this study we demonstrated that TA was effective in preventing SDAT in an icv-STZ model. TA prevents memory deficits, changes in AChE and NKA activities, and oxidative stress induced by STZ, which are symptoms associated with SAD. The icv-STZ (Salkovic-Petrisic et al.2013), non-transgenic metabolic model, employs icv injection of a diabetogenic toxin in the rat lateral ventricles. The key mechanism in the development of disease is the brain insulin resistance, as well as in the human SAD (Grieb 2016). Application of STZ leads to several brain metabolic and behavioral disturbances consequences of the decreased brain glucose utilization. This toxin also reduced ATP and energy charge potential in the cerebral cortex (Duelli et al.1994).