scholarly journals SWELLING OF FISH MITOCHONDRIA

1962 ◽  
Vol 13 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Thomas Richardson ◽  
A. L. Tappel
Keyword(s):  
Osmotic Pressure ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Rapid Rate ◽  
Mitochondrial Membranes ◽  
Fish Liver ◽  
Rapid Decay ◽  
Membrane Behavior ◽  
Slow Decay ◽  
Hypotonic Swelling

The physical properties of fish liver and rat liver mitochondria were compared as a function of temperature and osmotic pressure. The data indicate that fish mitochondria are more flexible and swell at a more rapid rate over a 0 to 30°C temperature range, whereas the rates of swelling at 30 to 40°C are comparable. The swelling rates of both fish and rat mitochondria vary with temperature and approximate the Arrhenius relationship. Apparent energies of activation for swelling averaged 26.5 kcal and 12.9 kcal for rat and fish, respectively. Fish mitochondria were less stable than rat mitochondria to osmotic variation, and the disparity in initial swelling rates became increasingly greater with lower osmotic pressure. The hypotonic swelling of both fish and rat mitochondria was readily reversed osmotically; however, there was a very rapid decay of reversal in fish mitochondria and only a very slow decay in the case of rat. All the data indicate that under comparable conditions the fish mitochondrial membranes are more flexible and presumably more permeable and labile than rat mitochondrial membranes. The findings are discussed in relation to the general metabolic implications and the possible contributions of the membrane constituents to membrane behavior.

scholarly journals Degradation of purines: only ureidoglycollate lyase out of four allantoin-degrading enzymes is present in mammals

1995 ◽  
Vol 312 (1) ◽  
pp. 315-318 ◽  
Author(s):  
S Fujiwara ◽  
T Noguchi
Keyword(s):  
Liver Enzyme ◽  
Rat Liver ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Mammalian Tissue ◽  
Mammalian Evolution ◽  
Fish Liver ◽  
Immunological Properties ◽  
Degrading Enzymes ◽  
Purine Degradation

It is generally accepted that all of the allantoin-degrading enzymes (allantoinase, allantoicase, ureidoglycollate lyase and urease), used in purine degradation, were lost during mammalian evolution. However, surprisingly, ureidoglycollate lyase has been found in a mammalian tissue. Ureidoglycollate lyase was purified to homogeneity and characterized from rat-liver mitochondria. The apparent Km (17 mM) of the rat enzyme for ureidoglycollate was much higher than that (0.33 mM) of fish-liver ureidoglycollate lyase. The rat-liver enzyme differed from the fish-liver enzyme in enzymic, physical and immunological properties.

scholarly journals ROLE OF EDTA AND METALS IN MITOCHONDRIAL CONTRACTION

1964 ◽  
Vol 23 (1) ◽  
pp. 9-19 ◽  
Author(s):  
William S. Lynn ◽  
Sydney Fortney ◽  
Rose H. Brown
Keyword(s):  
Atp Hydrolysis ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Matrix ◽  
Mitochondrial Membranes ◽  
Semipermeable Membranes ◽  
Microscopic Appearance ◽  
Hydration And Dehydration ◽  
Mitochondrial Contraction

Studies comparing the state of hydration and dehydration of rat liver mitochondria to their content of ATP, Ca, and fatty acid, along with the rate of ATP hydrolysis, as well as microscopic appearance of mitochondria, have led to the following generalizations: 1. The competition between cationic translocations and water translocation for the available chemical energy (ATP) determines under many circumstances the water content of mitochondria. 2. Swelling of mitochondria by electron transport substrates is an example of the activation of the cationic translocations at the expense of water translocation. 3. Electron micrographic studies are interpreted to indicate that EDTA alone can cause condensation and dehydration of the mitochondrial matrix. However, both EDTA and substrate are necessary to remove appreciable quantities of water from mitochondrial intramembranous spaces. 4. Since the data in the accompanying report indicated that EDTA, in the absence of energy, decreased the permeability of mitochondrial membranes, it appears likely that ballooning of intramembranous spaces, following addition of EDTA, represents trapping of water between two semipermeable membranes following dehydration of mitochondrial matrix.

scholarly journals INORGANIC PYROPHOSPHATASE OF RAT LIVER MITOCHONDRIA

1969 ◽  
Vol 42 (1) ◽  
pp. 235-240 ◽  
Author(s):  
Lloyd Schick ◽  
Larry G. Butler
Keyword(s):  
Rat Liver ◽  
Catalytic Properties ◽  
Liver Mitochondria ◽  
Inorganic Pyrophosphatase ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Membranes ◽  
Physiological Conditions ◽  
Enzyme Stimulation ◽  
Pyrophosphatase Activity ◽  
Stimulation Of

Stimulation of Mg2+-dependent inorganic pyrophosphatase activity several fold by disruption of mitochondrial membranes does not appreciably alter the catalytic properties of the enzyme. Stimulation is due to increased accessibility of substrate to the enzyme, which is not solublized on activation. The enzyme is attached to the inside of the inner membrane, and under physiological conditions probably hydrolyzes only intramitochondrially-produced PPi.

THE RESPIRATORY DEPENDENT SWELLING OF LIVER MITOCHONDRIA

1966 ◽  
Vol 44 (9) ◽  
pp. 1259-1270
Author(s):  
Roberto Cereijo-Santaló
Keyword(s):  
Reduced Glutathione ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Endogenous Respiration ◽  
Mitochondrial Membranes ◽  
Ph Values ◽  
Sucrose Medium ◽  
Lag Period ◽  
Ph Range ◽  
Reduced Nicotinamide Adenine Dinucleotide

The respiratory dependent swelling of isolated rat liver mitochondria was studied in sucrose and in potassium chloride media.In a sucrose medium it was found that mitochondria did not swell in the absence of respiration over the pH range 7.0–8.0. However, swelling of mitochondria readily occurred during the oxidation of endogenous or added respiratory substrates. Maximum rates of swelling at pH 7.0 were observed with ascorbate, reduced glutathione, and reduced nicotinamide–adenine dinucleotide (NADH). The swelling induced by substrate oxidation in a sucrose medium was markedly inhibited by the addition of KCl.In a KCl medium, mitochondria swelled in the absence of respiration at acid (6.0) and at alkaline (8.0) pH values, but were stable at pH 7.0–7.4. Endogenous respiration did not modify these results. The addition of β-hydroxybutyrate induced maximum swelling at pH 7.0. The extent of swelling produced by this substrate diminished when either the pH or the molarity of the buffer was increased. Ascorbate and reduced glutathione failed to induce swelling in a KCl medium. NADH in a KCl medium produced swelling to about the same extent as that in a sucrose medium. However, the onset of the swelling was delayed in the KCl medium. This lag period was shortened by the addition of rotenone and it was lengthened when either the molarity or the pH of the buffer was increased.An attempt has been made to relate these results to proton pressure produced in the mitochondrial membranes during electron transport.

Thyroid hormone and not growth hormone is the principle regulator of mammalian mitochondrial biogenesis

1989 ◽  
Vol 121 (2) ◽  
pp. 223-228 ◽  
Author(s):  
A. Mutvei ◽  
B. Husman ◽  
G. Andersson ◽  
B. D. Nelson
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormone ◽  
Mitochondrial Biogenesis ◽  
Binding Sites ◽  
Specific Binding ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Mitochondrial Membranes

Abstract. T3 and GH have been implicated in the regulation of mitochondrial biogenesis. Since thyroid hormone promotes the synthesis of growth hormone, its control of human mitochondrial biogenesis could arise through a permissive action on GH biosynthesis. This was studied in hypophysectomized rats treated with T3 and/or human GH by the continuous infusion of hormone for 6 days from mini-infusion pumps implanted sc. Increases in mitochondrial respiration, enzyme activites, and protein synthesis were found in isolated liver mitochondria from rats receiving T3. In contrast, GH alone had no effect, nor did it increase the response to T3. Since it has been argued that mitochondrial biogenesis results from a direct interaction (binding) of GH with mitochondria, GH-specific binding sites were measured with 125I-bGH, a specific somatogenic receptor ligand, in isolated mitochondrial membranes in vitro. In addition, the intracellular endocytic uptake of 125I-bGH injected in vivo was compared in purified subcellular membrane fractions and mitochondria. No evidence in favour of specific GH interaction on mitochondrial membranes was found by either test. It is concluded that T3 exerts a direct, rather than permissive, effect on mitochondrial biogenesis, and that high affinity binding sites for GH are not present in rat liver mitochondria.

Effects of 5-5'-Diphenyl-2-thiohydantoin (DPTH) and Thyroxine on the Ultrastructure and Chemical Composition of Rat Liver

1971 ◽  
Vol 29 ◽  
pp. 570-571
Author(s):  
E. A. Elfont ◽  
R. B. Tobin ◽  
D. G. Colton ◽  
M. A. Mehlman
Keyword(s):  
Chemical Composition ◽  
Rat Liver ◽  
Future Study ◽  
Mode Of Action ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Effective Inhibitor ◽  
Biochemical Effects ◽  
Glycerophosphate Dehydrogenase ◽  
Stimulation Of

Summary5,-5'-diphenyl-2-thiohydantoin (DPTH) is an effective inhibitor of thyroxine (T4) stimulation of α-glycerophosphate dehydrogenase in rat liver mitochondria. Because this finding indicated a possible tool for future study of the mode of action of thyroxine, the ultrastructural and biochemical effects of DPTH and/or thyroxine on rat liver mere investigated.Rats were fed either standard or DPTH (0.06%) diet for 30 days before T4 (250 ug/kg/day) was injected. Injection of T4 occurred daily for 10 days prior to sacrifice. After removal of the liver and kidneys, part of the tissue was frozen at -50°C for later biocheailcal analyses, while the rest was prefixed in buffered 3.5X glutaraldehyde (390 mOs) and post-fixed in buffered 1Z OsO4 (376 mOs). Tissues were embedded in Araldlte 502 and the sections examined in a Zeiss EM 9S.Hepatocytes from hyperthyroid rats (Fig. 2) demonstrated enlarged and more numerous mitochondria than those of controls (Fig. 1). Glycogen was almost totally absent from the cytoplasm of the T4-treated rats.

Two isoprenylated flavonoids from Dorstenia psilurus activate AMPK, stimulate glucose uptake, inhibit glucose production and lower glycemia

2019 ◽  
Vol 476 (24) ◽  
pp. 3687-3704 ◽  
Author(s):  
Aphrodite T. Choumessi ◽  
Manuel Johanns ◽  
Claire Beaufay ◽  
Marie-France Herent ◽  
Vincent Stroobant ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Human Cancer ◽  
Glucose Production ◽  
Liver Mitochondria ◽  
New Drugs ◽  
Structural Isomer ◽  
Rat Liver Mitochondria ◽  
Ionization Mass ◽  
Ampk Activation ◽  
Starting Point

Root extracts of a Cameroon medicinal plant, Dorstenia psilurus, were purified by screening for AMP-activated protein kinase (AMPK) activation in incubated mouse embryo fibroblasts (MEFs). Two isoprenylated flavones that activated AMPK were isolated. Compound 1 was identified as artelasticin by high-resolution electrospray ionization mass spectrometry and 2D-NMR while its structural isomer, compound 2, was isolated for the first time and differed only by the position of one double bond on one isoprenyl substituent. Treatment of MEFs with purified compound 1 or compound 2 led to rapid and robust AMPK activation at low micromolar concentrations and increased the intracellular AMP:ATP ratio. In oxygen consumption experiments on isolated rat liver mitochondria, compound 1 and compound 2 inhibited complex II of the electron transport chain and in freeze–thawed mitochondria succinate dehydrogenase was inhibited. In incubated rat skeletal muscles, both compounds activated AMPK and stimulated glucose uptake. Moreover, these effects were lost in muscles pre-incubated with AMPK inhibitor SBI-0206965, suggesting AMPK dependency. Incubation of mouse hepatocytes with compound 1 or compound 2 led to AMPK activation, but glucose production was decreased in hepatocytes from both wild-type and AMPKβ1−/− mice, suggesting that this effect was not AMPK-dependent. However, when administered intraperitoneally to high-fat diet-induced insulin-resistant mice, compound 1 and compound 2 had blood glucose-lowering effects. In addition, compound 1 and compound 2 reduced the viability of several human cancer cells in culture. The flavonoids we have identified could be a starting point for the development of new drugs to treat type 2 diabetes.

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