ROLE OF PHOSPHOLIPIDS IN MITOCHONDRIAL RESPIRATION

1959 ◽  
Vol 37 (8) ◽  
pp. 975-987 ◽  
Author(s):  
E. Petrushka ◽  
J. H. Quastel ◽  
P. G. Scholefield
Keyword(s):  
Rat Brain ◽  
Rat Liver ◽  
Snake Venom ◽  
Mitochondrial Respiration ◽  
Rat Kidney ◽  
Protective Action ◽  
Brain Mitochondria ◽  
Phospholipase A ◽  
Inhibitory Effects ◽  
Cortex Slices

The addition of heated snake venom solutions to suspensions of rat liver, kidney, or brain mitochondria results in an initial stimulation of the rate of respiration, which is approximately the same for a variety of substrates, followed by a rapid decline.The presence of phospholipase A in heated snake venom is demonstrated by the formation of lysolecithin from mitochondrial lecithin. Various phospholipids, when added to mitochondria, have a protective influence against the inhibitory effects of phospholipase of heated venoms on respiration. Clostridium welchii toxin, which contains phospholipase C, has an effect on mitochondrial respiration which is similar to that of venom phospholipase A but the addition of phospholipid has no protective effect.Glutathione exercises a protective action against the inhibitory effects of phospholipase A on rat liver or kidney mitochondrial respiration, the action consisting of a prolongation of the initial stimulated phase of respiration. The effect does not seem to obtain with rat brain mitochondria.Exposure of rat brain cortex slices, but not those of rat kidney or liver, to heated venom results in changes of respiratory rates similar to those obtained with brain mitochondria.

ROLE OF PHOSPHOLIPIDS IN MITOCHONDRIAL RESPIRATION

1959 ◽  
Vol 37 (1) ◽  
pp. 975-987 ◽  
Author(s):  
E. Petrushka ◽  
J. H. Quastel ◽  
P. G. Scholefield
Keyword(s):  
Rat Brain ◽  
Rat Liver ◽  
Snake Venom ◽  
Mitochondrial Respiration ◽  
Rat Kidney ◽  
Protective Action ◽  
Brain Mitochondria ◽  
Phospholipase A ◽  
Inhibitory Effects ◽  
Cortex Slices

The addition of heated snake venom solutions to suspensions of rat liver, kidney, or brain mitochondria results in an initial stimulation of the rate of respiration, which is approximately the same for a variety of substrates, followed by a rapid decline.The presence of phospholipase A in heated snake venom is demonstrated by the formation of lysolecithin from mitochondrial lecithin. Various phospholipids, when added to mitochondria, have a protective influence against the inhibitory effects of phospholipase of heated venoms on respiration. Clostridium welchii toxin, which contains phospholipase C, has an effect on mitochondrial respiration which is similar to that of venom phospholipase A but the addition of phospholipid has no protective effect.Glutathione exercises a protective action against the inhibitory effects of phospholipase A on rat liver or kidney mitochondrial respiration, the action consisting of a prolongation of the initial stimulated phase of respiration. The effect does not seem to obtain with rat brain mitochondria.Exposure of rat brain cortex slices, but not those of rat kidney or liver, to heated venom results in changes of respiratory rates similar to those obtained with brain mitochondria.

THE EFFECTS OF ALIPHATIC ALDEHYDES ON THE RESPIRATION OF RAT BRAIN CORTEX SLICES AND RAT BRAIN MITOCHONDRIA

1958 ◽  
Vol 36 (6) ◽  
pp. 531-541 ◽  
Author(s):  
C. T. Beer ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Mitochondrial Respiration ◽  
Brain Cortex ◽  
Brain Mitochondria ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Low Concentrations ◽  
Brain Cortex Slices ◽  
Cortex Slices

A study has been made of the effects of acetaldehyde and n-valeric aldehyde on the respiration of rat brain cortex slices in the presence and absence of 0.1 M KCl. Acetaldehyde at low concentrations (1–2 mM) brings about a marked inhibition of potassium-stimulated respiration of brain cortex slices. The inhibition by acetaldehyde occurs at 1/200th the concentration at which ethanol produces the same effects. The stimulation of brain respiration due to potassium ions is abolished by acetaldehyde at concentrations that have no observable effect on the unstimulated respiration. Acetaldehyde and n-valeric aldehyde, at equivalent concentrations, have almost equal inhibitory effects on potassium-stimulated rat brain cortex respiration. The inhibitory effects of the aldehydes do not increase sharply with increase of their concentrations, in contrast to the effects of the corresponding alcohols. The aldehydes, in contrast to the corresponding alcohols, inhibit brain mitochondrial respiration as markedly as they inhibit brain cortex respiration. The inhibitory effect of the aldehyde on mitochondrial respiration with pyruvate as substrate is greater in the presence of small quantities of malate than in the absence of malate. The acetaldehyde inhibition is abolished on the addition of DPN. The results obtained with the aldehydes do not support the view that the corresponding alcohols exercise their inhibitive effects on brain respiration by preliminary conversion to the aldehydes. It is suggested that the aldehydes exercise their inhibitory effects on brain respiration by rapid attainment of equilibrium with a constituent of the brain respiratory system associated with a rate-limiting step in the citric acid cycle.

THE EFFECTS OF ALIPHATIC ALDEHYDES ON THE RESPIRATION OF RAT BRAIN CORTEX SLICES AND RAT BRAIN MITOCHONDRIA

1958 ◽  
Vol 36 (1) ◽  
pp. 531-541 ◽  
Author(s):  
C. T. Beer ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Mitochondrial Respiration ◽  
Brain Cortex ◽  
Brain Mitochondria ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Low Concentrations ◽  
Brain Cortex Slices ◽  
Cortex Slices

A study has been made of the effects of acetaldehyde and n-valeric aldehyde on the respiration of rat brain cortex slices in the presence and absence of 0.1 M KCl. Acetaldehyde at low concentrations (1–2 mM) brings about a marked inhibition of potassium-stimulated respiration of brain cortex slices. The inhibition by acetaldehyde occurs at 1/200th the concentration at which ethanol produces the same effects. The stimulation of brain respiration due to potassium ions is abolished by acetaldehyde at concentrations that have no observable effect on the unstimulated respiration. Acetaldehyde and n-valeric aldehyde, at equivalent concentrations, have almost equal inhibitory effects on potassium-stimulated rat brain cortex respiration. The inhibitory effects of the aldehydes do not increase sharply with increase of their concentrations, in contrast to the effects of the corresponding alcohols. The aldehydes, in contrast to the corresponding alcohols, inhibit brain mitochondrial respiration as markedly as they inhibit brain cortex respiration. The inhibitory effect of the aldehyde on mitochondrial respiration with pyruvate as substrate is greater in the presence of small quantities of malate than in the absence of malate. The acetaldehyde inhibition is abolished on the addition of DPN. The results obtained with the aldehydes do not support the view that the corresponding alcohols exercise their inhibitive effects on brain respiration by preliminary conversion to the aldehydes. It is suggested that the aldehydes exercise their inhibitory effects on brain respiration by rapid attainment of equilibrium with a constituent of the brain respiratory system associated with a rate-limiting step in the citric acid cycle.

BIOCHEMICAL STUDIES ON TOFRANIL

1961 ◽  
Vol 39 (3) ◽  
pp. 551-558 ◽  
Author(s):  
P. N. Abadom ◽  
K. Ahmed ◽  
P. G. Scholefield
Keyword(s):  
Rat Brain ◽  
Rat Liver ◽  
Brain Cortex ◽  
Respiratory Activity ◽  
Liver Mitochondria ◽  
Brain Mitochondria ◽  
Inhibitory Effect ◽  
Rat Liver Mitochondria ◽  
Brain Cortex Slices ◽  
Cortex Slices

Tofranil inhibits the respiratory activity of rat brain cortex slices incubated in a glucose-containing medium. It also inhibits the uptake and incorporation of glycine-1-C14at concentrations which have only a slight inhibitory effect on the respiration of slices. Tofranil also inhibits oxidative phosphorylation in both rat liver and rat brain mitochondria but at higher concentrations respiration is greatly affected. Tofranil differs quantitatively from chlorpromazine in its greater inhibitory effect on the ATP–Pi32exchange reaction and its lesser effect on the cytochrome c oxidase activity of rat liver mitochondria.

THE EFFECTS OF ALIPHATIC ALCOHOLS ON THE RESPIRATION OF RAT BRAIN CORTEX SLICES AND RAT BRAIN MITOCHONDRIA

1958 ◽  
Vol 36 (6) ◽  
pp. 543-556 ◽  
Author(s):  
C. T. Beer ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Brain Mitochondria ◽  
Carbon Chain ◽  
Brain Cell ◽  
Aliphatic Alcohols ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

A study has been made of the effects of a series of aliphatic alcohols (ethanol, n-propanol, isopropanol, n-butanol, and n-pentanol) on the respiration of rat brain cortex slices in the presence or absence of 0.1 M KCl. The respiration of rat brain cortex slices incubated in presence of 0.1 M KCl is found to be much more sensitive to the alcohols than that of the tissue incubated in absence of the added potassium ions. The inhibitory effects of the alcohols increase markedly as the length of the carbon chain increases and with increase of their concentrations. The stimulation of brain cortex respiration by addition of 0.1 M KCl is diminished or abolished by concentrations of the alcohols that have little effect on the unstimulated respiration. n-Pentanol is far more effective than ethanol in effecting an inhibition of potassium-stimulated brain cortex respiration. The inhibitive effects of the alcohols at low concentration on potassium-stimulated brain cortex respiration are not due to a gradual denaturation of tissue proteins. The data point to a rapid establishment of equilibria between the alcohols and components influencing brain respiratory systems. Brain mitochondrial respiration is relatively insensitive to concentrations of alcohols that considerably depress potassium-stimulated respiration of rat brain cortex slices. It is suggested that the alcohols exercise their inhibitory effects on brain cortex respiration at the brain cell membranes.

THE EFFECTS OF ALIPHATIC ALCOHOLS ON THE RESPIRATION OF RAT BRAIN CORTEX SLICES AND RAT BRAIN MITOCHONDRIA

1958 ◽  
Vol 36 (1) ◽  
pp. 543-556 ◽  
Author(s):  
C. T. Beer ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Brain Mitochondria ◽  
Carbon Chain ◽  
Brain Cell ◽  
Aliphatic Alcohols ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

A study has been made of the effects of a series of aliphatic alcohols (ethanol, n-propanol, isopropanol, n-butanol, and n-pentanol) on the respiration of rat brain cortex slices in the presence or absence of 0.1 M KCl. The respiration of rat brain cortex slices incubated in presence of 0.1 M KCl is found to be much more sensitive to the alcohols than that of the tissue incubated in absence of the added potassium ions. The inhibitory effects of the alcohols increase markedly as the length of the carbon chain increases and with increase of their concentrations. The stimulation of brain cortex respiration by addition of 0.1 M KCl is diminished or abolished by concentrations of the alcohols that have little effect on the unstimulated respiration. n-Pentanol is far more effective than ethanol in effecting an inhibition of potassium-stimulated brain cortex respiration. The inhibitive effects of the alcohols at low concentration on potassium-stimulated brain cortex respiration are not due to a gradual denaturation of tissue proteins. The data point to a rapid establishment of equilibria between the alcohols and components influencing brain respiratory systems. Brain mitochondrial respiration is relatively insensitive to concentrations of alcohols that considerably depress potassium-stimulated respiration of rat brain cortex slices. It is suggested that the alcohols exercise their inhibitory effects on brain cortex respiration at the brain cell membranes.

STUDIES OF FATTY ACID OXIDATION: 4. THE EFFECTS OF FATTY ACIDS ON THE OXIDATION OF OTHER METABOLITES

1956 ◽  
Vol 34 (6) ◽  
pp. 1211-1225 ◽  
Author(s):  
P. G. Scholefield
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Respiratory Activity ◽  
Tricarboxylic Acid Cycle ◽  
Rat Kidney ◽  
Brain Mitochondria ◽  
Acid Oxidation ◽  
Inhibitory Effects ◽  
Kidney Mitochondria ◽  
Low Concentrations

Fatty acids inhibit the oxidation of pyruvate by rat-kidney mitochondria but the extent of inhibition depends upon the nature and amount of agent added to stimulate the oxidation. The longer chain fatty acids are more effective inhibitors and, in general, the even-numbered fatty acids show greater inhibitory effects than the adjacent odd-numbered fatty acids. Under conditions where 2, 4-dinitrophenol (DNOP) and the fatty acids separately have little effect on the respiratory activity of rat-kidney mitochondria with pyruvate as substrate, the addition of both fatty acid and DNOP results in an extensive inhibition. At low concentrations the fatty acids are oxidized by rat-kidney mitochondria but at concentrations of 10−3 M and higher they inhibit their own oxidation, the oxidation of pyruvate, and those of the acids of the tricarboxylic acid cycle. The oxidation of pyruvate by rat-brain mitochondria is insensitive to decanoate but both the fumarate- and DNOP-stimulated oxidations of pyruvate are sensitive to the presence of decanoate. In contrast, Nembutal inhibits both the oxidation of pyruvate alone and the fumarate-stimulated oxidation of pyruvate. Possible mechanisms for the observed inhibitory effects of fatty acids are discussed.

Characterization of rat iodothyronine sulfotransferases

2003 ◽  
Vol 285 (3) ◽  
pp. E592-E598 ◽  
Author(s):  
Monique H. A. Kester ◽  
Ellen Kaptein ◽  
Thirza J. Roest ◽  
Caren H. van Dijk ◽  
Dick Tibboel ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Rat Brain ◽  
Rat Liver ◽  
Rat Kidney ◽  
Female Rat ◽  
Reversible Inactivation ◽  
Fetal Thyroid ◽  
Important Pathway ◽  
Brain Cytosol

Sulfation appears to be an important pathway for the reversible inactivation of thyroid hormone during fetal development. The rat is an often used animal model to study the regulation of fetal thyroid hormone status. The present study was done to determine which sulfotransferases (SULTs) are important for iodothyronine sulfation in the rat, using radioactive T4, T3, rT3, and 3,3′-T2 as substrates, 3′-phosphoadenosine-5′-phosphosulfate (PAPS) as cofactor, and rat liver, kidney and brain cytosol, and recombinant rat SULT1A1, -1B1, -1C1, -1E1, -2A1, -2A2, and -2A3 as enzymes. Recombinant rat SULT1A1, -1E1, -2A1, -2A2, and -2A3 failed to catalyze iodothyronine sulfation. For all tissue SULTs and for rSULT1B1 and rSULT1C1, 3,3′-T2 was by far the preferred substrate. Apparent Km values for 3,3′-T2 amounted to 1.9 μM in male liver, 4.4 μM in female liver, 0.76 μM in male kidney, 0.23 μM in male brain, 7.7 μM for SULT1B1, and 0.62 μM for SULT1C1, whereas apparent Km values for PAPS showed less variation (2.0-6.9 μM). Sulfation of 3,3′-T2 was inhibited dose dependently by other iodothyronines, with similar structure-activity relationships for most enzymes except for the SULT activity in rat brain. The apparent Km values of 3,3′-T2 in liver cytosol were between those determined for SULT1B1 and -1C1, supporting the importance of these enzymes for the sulfation of iodothyronines in rat liver, with a greater contribution of SULT1C1 in male than in female rat liver. The results further suggest that rSULT1C1 also contributes to iodothyronine sulfation in rat kidney, whereas other, yet-unidentified forms appear more important for the sulfation of thyroid hormone in rat brain.

AMINO ACID TRANSPORT IN BRAIN CORTEX SLICES: II. COMPETITION BETWEEN AMINO ACIDS

1962 ◽  
Vol 40 (11) ◽  
pp. 1591-1602 ◽  
Author(s):  
P. N. Abadom ◽  
P. G. Scholefield
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Rat Brain ◽  
Amino Acid Transport ◽  
Brain Cortex ◽  
Transport Systems ◽  
Acid Transport ◽  
Inhibitory Effects ◽  
Brain Cortex Slices ◽  
Cortex Slices

Evidence is presented which indicates that several amino acid transport systems are present in rat brain cortex slices, each with its own specificity with regard to substrate and with regard to amino acids which produce inhibitory effects. The nature of these inhibitory effects may be either direct (competition for a limiting number of sites) or indirect (as they are when glutamate or aspartate cause a decrease in the ATP content).Comparison of the specificities of the glycine transport systems present in rat brain cortex slices and in Ehrlich ascites carcinoma cells indicates that these two systems have little in common and the relation of this finding to the structural requirements necessary for chemotherapeutic activity is discussed.

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