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Role of Mitochondrial Injury During Oxidative Injury to Hepatocytes: Evidence of a Mitochondrial Permeability Transition by Laser Scanning Confocal Microscopy
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Anna-Liisa Nieminen, Roberto Imberti, Alice K. Saylor, Samuel A. Tesfai, Brian Herman, John J. Lemasters
We also investigated the ability of fructose to protect against hepatocellular injury by Br-A23187. Br-A23187 and its parent compound, A23187, are calcium ionophores whose cytotoxicity is sometimes used as a model of Ca2+-dependent cell killing.10 Br-A23187 caused time-dependent killing of isolated hepatocytes, and virtually all cells were nonviable after 2 h of exposure (Figure 4). Fructose alone only slightly improved cell survival, but fructose in combination with oligomycin virtually eliminated cell killing. Cell killing by CCCP showed the same pattern of oligomycin and fructose-dependent protection (Figure 4). These observations indicated that mitochondrial uncoupling and accelerated ATP hydrolysis were causing lethal cell injury from Br-A23187, rather than increases of intracellular Ca2+ per se. This is consistent with observations in isolated mitochondria, where A23187 is well known to be an uncoupler.11
Ultrastructure of The Myometrium and The role of Gap Junctions in Myometrial Function
Published in Gabor Huszar, The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Arie Verhoeff, Robert E. Garfield
Recently it has become apparent that cells connected by gap junctions may not necessarily show a free exchange of dyes, isotopes, and current.41,42,44,46,50 Electrophysiologic studies show that gap junctions can rapidly switch from a low to a high resistance.44,46 It is now recognized that the channels or pores created by the gap junction may not always be in the open state.44,46,51,52 There may be times when the channels are open and times when they are closed. This uncoupling mechanism may be a safety device to uncouple injured cells44 or to uncouple cells when metabolically or electrically desirable. Closing the channels or uncoupling has been achieved by changes in internal and external Ca++ and pH.41,44,46,50-52
Heat Shock Proteins and Cell Thermotolerance
Published in Leopold J. Anghileri, Jacques Robert, Hyperthermia In Cancer Treatment, 2019
In view of these findings, subsequent studies have addressed the question as to whether chemical agents known to induce thermotolerance would also generate HSP production, and conversely, whether known inducers or inhibitors of HSP synthesis would similarly affect thermotolerance development. In agreement with the concept that HSP are causal in the development of thermotolerance, it was found that ethanol, a well-characterized thermotolerance inducer,73 was indeed a potent inducer of HSP, starting at the concentration that induces thermotolerance.18,74 Also, a large number of agents reported to induce HSP or chromosomal puffing in Drosophila (see reviews by Ashburner and Bonner40 and by Tanguay42) were reported to induce thermotolerance. Figure 4 shows the results of an experiment where the effect of varying concentrations of carbonyl cyanide m-chlorophenylhydrazone (CCCP) on HSP and thermotolerance induction was studied in a normal, low-differentiated epithelial cell line from rat liver. It is demonstrated that the two responses are triggered by the uncoupler, starting in both cases at a concentration of about 100 µM. A similar coordinated induction of HSP and thermotolerance was demonstrated in other cell lines following recovery from hypoxia or glucose deprivation, or treatment with CCCP, dinitriphenol, disulfiram, and arsenite.16,66,74,76,101 In Morris hepatoma cells, however, arsenite did not seem to induce thermotolerance in spite of a strong synthesis of HSP.18 This point will be further discussed below.
Cold stored platelets in the management of bleeding: is it about bioenergetics?
Published in Platelets, 2023
Chloe E. George, Christine V. Saunders, Alex Morrison, Tom Scorer, Sarah Jones, Nina C. Dempsey
The use of modulators of the ETC in the XF analyzer has the potential to provide a more precise understanding of platelet concentrate metabolism during storage through the isolation of individual parts of the ETC. The use of the inhibitor oligomycin inhibits ATP synthase, resulting in a reduction in the OCR that reflects the fraction of oxygen consumption as a result of ATP synthesis via OXPHOS. The subsequent addition of rotenone (a complex I inhibitor) and antimycin A (a complex III inhibitor) shuts down mitochondrial respiration and, with the simultaneous measurement of the acidification rate, enables the calculation of glycolysis-driven ATP production [87]. The respiratory reserve of mitochondria can be measured with the addition of a proton uncoupler, which allows protons to bypass the ATP synthase and consume oxygen at the maximum potential rate. By subtracting the basal OCR from this maximal rate, it is possible to quantify the ability of the cells to respond to a stressor with increased ATP production [88].
Chemotherapeutic and prophylactic antimalarial drugs induce cell death through mitochondrial-mediated apoptosis in murine models
Published in Drug and Chemical Toxicology, 2021
John Oludele Olanlokun, Folashade Abimbola Balogun, Olufunso Olabode Olorunsogo
The method of Lardy and Wellman (1953) was used. To each test tube in duplicate, 0.25 M sucrose, 5 mM KCl, 0.1 M Tris-HCl (pH 7.4) were added to all test tubes containing mitochondria (1 mg/mL protein) and the volumes were made up to 2 mL. Uncoupler (25 µM 2, 4 dinitrophenol) was added to the designated tubes followed by 0.01 M ATP. Sodium dodecylsulphate (SDS, 10% w/v) was added to the tubes designated zero time tubes after the addition of mitochondria. After adding ATP, mitochondria were added to each test tube at 30 seconds interval in a shaking water bath at 27 °C. The mixture was incubated for 30 minutes. After incubation, 1 mL of SDS was added to each test tube (except zero time) at 30 seconds interval in the order mitochondria were added to terminate the reaction. Ammonium molybdate (1 mL of 1.25% (w/v) in 6.25% H2SO4 preparation) was added to each test tube followed by 1 mL (9% w/v) of ascorbate. The solutions were allowed to stand for 30 minutes and absorbance was read at 680 nm. The inorganic phosphate (Pi) concentration was obtained from a phosphate standard curve.
Comparative effects of galactose-induced aging on mitochondrial permeability transition in rat liver and testis
Published in Toxicology Mechanisms and Methods, 2020
Olubukola T. Oyebode, Olawumi D. Giwa, Olufunso O. Olorunsogo
The effects of galactose administration on mitochondrial ATPase activity at physiological pH (7.4) and levels of lipid peroxides are depicted in Figure 3. Rat liver mitochondrial ATPase activity was significantly enhanced at physiological pH (7.4) by administration of galactose (50–500 mg/kg) by 1.6, 2.2, 2.7, and 2.3 folds, respectively. The highest enhancement fold obtained (2.7) was close to that observed with 2, 4-dinitrophenol (3.3), a standard uncoupler of oxidative phosphorylation. However, there was no significant effect of galactose administration in the testis at all doses administered. Furthermore, levels of mitochondrial MDA in the liver were significantly (p < 0.001) increased up to 4 folds at 500 mg/kg in the liver of galactose-induced aging rats. However, there was no significant elevation at 50 mg/kg. In the testis, minimal increases in MDA levels were observed which were lower when compared to effects seen in the liver.