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(Poly)phenols in Exercise Performance and Recovery
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Another mechanism by which (poly)phenols might enhance exercise performance is by augmenting mitochondrial biogenesis. Rodent and in vitro studies have found that (poly)phenols activate two important molecular pathways for mitochondrial biogenesis, sirtuin-1 (SIRT 1) and peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC1α) (Sandoval-Acuña, Ferreira and Speisky, 2014). In a rodent study, the polyphenol quercetin increased cytochrome C enzyme concentration, a marker of mitochondrial biogenesis, and this was paralleled by improvements in exercise performance (Davis et al., 2009). Follow-up studies with more valid markers of mitochondrial biogenesis such as citrate synthase activity and cardiolipin content (Larsen et al., 2012) are still needed. Similar ergogenic effects have been reported with green tea catechins (Murase et al., 2006). However, aside from one study with quercetin (Nieman et al., 2010), there is currently little evidence that (poly)phenols enhance mitochondrial biogenesis in humans.
Neurotransmission at Parasympathetic Nerve Endings
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
The AcCoA substrate is formed in the mitochondria, the membrane of which is relatively impermeable. It therefore has to pass to the cytoplasm in the form of pyruvate, citrate or acetate depending upon the location of the nerve. AcCoA is then reformed. Pyruvate is generated within the mitochondria by the action of pyruvate dehydrogenase. Citrate is derived from oxaloacetic acetate and AcCoA by citrate synthase and transported from the mitochondria. AcCoA is produced in the cytoplasm from citrate and ATP by the action of ATP citrate lysase. Acetate reacts with ATP under the influence of acetate thiokinase to form an enzyme-bound acetyl AMP, which in the presence of CoA undergoes transacetylation to form AcCoA.
The Microenvironment in Multicellular Spheroids
Published in Rolf Bjerkvig, Spheroid Culture in Cancer Research, 2017
Determinations of the citrate-synthase activity of the two tumor cell lines gave the value 113.6 mU/mg for HT-29 cells and 44.5 mU/mg for U-118MG cells (p ≤ 0.01).33 These data can be interpreted as if the LDH activity in HT-29 cells was, due to the high affinity (low km value), already saturated at low pyruvate concentrations. The activity of the citric cycle with the high citrate-synthase activity could be easily enhanced by a further increase of the pyruvate concentration, giving a high oxygen consumption. The U-118MG cells seemed to have less active citric cycle activity, but a higher pyruvate turnover rate, giving high lactate production. The competition for NADH+, H+ between LDH and the citric cycle could possibly act as a control determining the activity of both degradation pathways.
Effects of different standard and special diets on cognition and brain mitochondrial function in mice
Published in Nutritional Neuroscience, 2022
Martina Reutzel, Rekha Grewal, Carsten Esselun, Sebastian Friedrich Petry, Thomas Linn, Annette Brandt, Ina Bergheim, Gunter P. Eckert
Basal ATP-levels were measured in dissociated brain cells (DBC’s) of mice fed with AC1000, AC1000mod or Acont (Figure 3(a)). The AC1000mod diet lead to a significant increase in basal ATP levels compared to AC1000 fed animals (Figure 3(a)). The mitochondrial membrane potential (MMP) did not show any differences between all three considered groups (Figure 3(b)). Mitochondrial respiration was measured in isolated brain mitochondria from AC1000, AC1000mod or Acont fed mice. (Figure 3(c)). Citrate synthase activity, a well-established marker for mitochondrial mass, was determined in isolated mitochondria [18]. AC1000mod fed mice showed a significant decrease in CS activity compared to mice which received the Acont diet (Figure 3(d)).
Identification of a new structural family of SGK1 inhibitors as potential neuroprotective agents
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Ines Maestro, Enrique Madruga, Patricia Boya, Ana Martínez
We confirmed this effect in the neuroblastoma cellular line SH-SY5Y. For that, the activity of the enzyme citrate synthase was determined. This enzyme participates in the Kreb’s cycle and its activity can be used to measure the amount of mitochondria in a sample. Cells were treated with the inducer DFP and the compounds GSK650394 and AEV1.40. Data showed a decrease in citrate synthase activity when cells were treated with the enhancer DFP, as it reduces the amount of mitochondria by mitophagy. In addition, the co-treatment with the inhibitor of SGK1, GSK650394, significatively recovered the loss of mitochondria to control levels. The compound AEV1.40 showed a similar tendency than GSK650394, increasing the activity of the citrate synthase (Figure 10).
miRNA-378a as a key regulator of cardiovascular health following engineered nanomaterial inhalation exposure
Published in Nanotoxicology, 2019
Quincy A. Hathaway, Andrya J. Durr, Danielle L. Shepherd, Mark V. Pinti, Ashley N. Brandebura, Cody E. Nichols, Amina Kunovac, William T. Goldsmith, Sherri A. Friend, Alaeddin B. Abukabda, Garrett K. Fink, Timothy R. Nurkiewicz, John M. Hollander
Citrate synthase is key to metabolism through the production of citrate from acetyl-CoA and oxaloacetate, initiating the tricarboxylic acid cycle. To determine the number of mitochondria in heart tissue, a colorimetric Citrate Synthase Assay (Sciencell, San Diego, CA) was employed per manufacturer’s instructions (Jagannathan et al. 2015). The Bradford method (Bradford 1976), with standardization to bovine serum albumin, provided normalization of protein concentrations for cardiac mitochondria. Briefly, 1 µg of mitochondria was used to measure the colorimetric change produced from 5′, 5′-Dithiobis 2-nitrobenzoic acid and CoA-SH forming of TNB at an absorbance maximum of 412 nm.