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.

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.

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.

UPTAKE OF 5-HYDROXYTRYPTOPHAN-3-C14 AND ITS METABOLISM IN RAT BRAIN CORTEX SLICES

1962 ◽  
Vol 40 (1) ◽  
pp. 1439-1448
Author(s):  
J. P. von Wartburg
Keyword(s):  
Monoamine Oxidase ◽  
Synergistic Effect ◽  
Rat Brain ◽  
Brain Cortex ◽  
Brain Slices ◽  
Inhibitory Effect ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

Rat brain cortex slices were incubated with 5-hydroxytryptophan-3-C14. A method for determination of 5-hydroxytryptamine-C14 and 5-hydroxyindolacetic acid-C14 formed in brain slices is described. Effects of inhibitors of 5-hydroxytryptophan decarboxylase and monoamine oxidase on the metabolic pathway of 5-hydroxytryptophan-3-C14 were measured. α-Methyl dopa (0.33 mM) decreased the level of 5-hydroxyindolacetic acid to a greater amount than that of 5-hydroxytryptamine. Iproniazid (3.3 mM) resulted in an accumulation of 5-hydroxytryptamine and a decrease of 5-hydroxyindolacetic acid formation of 65%. Pheniprazine (0.1 mM) exerted an inhibitory effect on both 5-hydroxytryptophan decarboxylase and monoamine oxidase. Chlorpromazine (0.5 mM) decreased the level of 5-hydroxytryptamine 60% and had a synergistic effect with the inhibition on respiration of brain slices and 5-hydroxytryptophan transport exerted by 0.2 M n-propanol.

UPTAKE OF 5-HYDROXYTRYPTOPHAN-3-C14 AND ITS METABOLISM IN RAT BRAIN CORTEX SLICES

1962 ◽  
Vol 40 (10) ◽  
pp. 1439-1448 ◽  
Author(s):  
J. P. von Wartburg
Keyword(s):  
Monoamine Oxidase ◽  
Synergistic Effect ◽  
Rat Brain ◽  
Brain Cortex ◽  
Brain Slices ◽  
Inhibitory Effect ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

Rat brain cortex slices were incubated with 5-hydroxytryptophan-3-C14. A method for determination of 5-hydroxytryptamine-C14 and 5-hydroxyindolacetic acid-C14 formed in brain slices is described. Effects of inhibitors of 5-hydroxytryptophan decarboxylase and monoamine oxidase on the metabolic pathway of 5-hydroxytryptophan-3-C14 were measured. α-Methyl dopa (0.33 mM) decreased the level of 5-hydroxyindolacetic acid to a greater amount than that of 5-hydroxytryptamine. Iproniazid (3.3 mM) resulted in an accumulation of 5-hydroxytryptamine and a decrease of 5-hydroxyindolacetic acid formation of 65%. Pheniprazine (0.1 mM) exerted an inhibitory effect on both 5-hydroxytryptophan decarboxylase and monoamine oxidase. Chlorpromazine (0.5 mM) decreased the level of 5-hydroxytryptamine 60% and had a synergistic effect with the inhibition on respiration of brain slices and 5-hydroxytryptophan transport exerted by 0.2 M n-propanol.

EFFECTS OF ALIPHATIC ALCOHOLS AND ALDEHYDES ON THE METABOLISM OF POTASSIUM-STIMULATED RAT BRAIN CORTEX SLICES

1965 ◽  
Vol 43 (7) ◽  
pp. 1041-1051 ◽  
Author(s):  
Edward Majchrowicz
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Brain Slices ◽  
Carbon Chain ◽  
Aliphatic Alcohols ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
The Brain

Aliphatic alcohols and the corresponding aldehydes inhibit the oxidation of glucose-U-C14to C14O2, total respiratory carbon dioxide formation, and oxygen consumption by potassium-stimulated rat brain cortex slices. The inhibitory effects of alcohols increase with the increase of the length of carbon chain, which is similar to the inhibitory effects of alcohols on the metabolism of liver slices. Forty millimolar pentanol and ethanol inhibit C14O2formation by 92% and 17% respectively. However, aliphatic alcohols at a fraction of the concentrations used with brain slices severely suppress C14O2formation, total CO2formation, and incorporation of acetate-1-C14and glucose-U-C14into hepatic lipids and proteins.At low concentrations aldehyde inhibition increases rapidly with the concentration, which is in direct contrast to ethanol or propanol whose inhibitory effects change slightly. Three millimolar propionaldehyde, butyraldehyde, and valeraldehyde are approximately 6 times more inhibitory to C14O2formation than the corresponding alcohols at 20 mM; acetaldehyde (3 mM), on the other hand, is approximately 24 times more inhibitory than 20 mM ethanol. These observations show that aldehydes affect the metabolism of brain slices in a different manner than the corresponding alcohols, which is consistent with the conclusion that there is no enzyme system present in the brain cortex slices responsible for the oxidation of alcohols to aldehydes. In contrast to aliphatic alcohols, the inhibitory effects of aldehydes do not increase with the length of aliphatic carbon chain. Of all alcohols and aldehydes tested, the inhibitions caused by acetaldehyde and valeraldehyde are most severe and approximately equal at equivalent concentrations. Three millimolar acetaldehyde and valeraldehyde suppress C14O2formation by 58% and 53% respectively. The effects of 3 mM propionaldehyde and butyraldehyde (29% and 26% respectively) are also approximately equal but smaller than those of either acetaldehyde or valeraldehyde.The observed inhibitory effects of alcohols on the metabolism of rat brain cortex slices support the suggestion that the site of ethanol inhibition is partly associated with that component of the oxidative system which is dependent on normal functioning of the active transport of sodium across the nerve cell membrane and partly due to acetaldehyde which is conveyed via the blood stream from liver to the brain. Similar deductions may apply to other aliphatic alcohols. The inhibitory effects of aldehydes are consistent with the conclusion that the inhibition depends on the properties of the aldehyde group rather than on the length of carbon chain, although their effects on ion transport across the nerve cell membrane have yet to be reported.

EFFECTS OF ACETYLSALICYLATE AND 2,4-DINITROPHENOL ON METABOLISM AND TRANSPORT IN RAT BRAIN CORTEX IN VITRO

1963 ◽  
Vol 41 (2) ◽  
pp. 435-454 ◽  
Author(s):  
O. Gonda ◽  
J. H. Quastel
Keyword(s):  
Amino Acids ◽  
Rat Brain ◽  
Brain Cortex ◽  
Transport Processes ◽  
Rat Brain Cortex ◽  
High K ◽  
Increased Sensitivity ◽  
Brain Cortex Slices ◽  
Cortex Slices

The effects of acetylsalicylate and of 2,4-dinitrophenol on the metabolism and transport processes of rat brain cortex slices incubated at 37° in glucose–Ringer media under various conditions have been investigated. The following processes are suppressed by acetylsalicylate (5 mM) or dinitrophenol (0.05 mM) to a much greater extent in media containing 105 mM KCl or 10 mM NH4Cl (which stimulate brain respiration) than in normal media:(a) respiration;(b) incorporation of phosphate into ATP and ADP;(c) conversion of creatine to phosphocreatine;(d) uptake of glutamate or of creatine from the medium to the tissue.The two drugs increase the leakage of amino acids from rat brain cortex slices into the medium, the effects being greatest in the presence of 105 mM KCl or 5 mM glutamate or in the absence of glucose. They change the yields of labelled amino acids from labelled glucose or labelled glutamate.Labelled glutamate is converted to labelled aspartate, γ-aminobutyrate and glutamine in rat brain cortex slices, the addition of glucose bringing about increased yields of glutamine and γ-aminobutyrate and a decreased yield of aspartate. The formation of labelled glutamine from either labelled glutamate or from labelled glucose is suppressed by acetylsalicylate or dinitrophenol, the effects being greater in the presence of 105 mM KCl or 10 mM NH4Cl.The increased sensitivity of the stimulated tissue metabolism to the drugs, in the presence of high K+, or of NH4+or of glutamate, is probably explained by the fact that there is a fall, under these conditions, in the tissue phosphocreatine level. There is, therefore, less reserve phosphocreatine to maintain the level of ATP when neuronal oxidative phosphorylation is suppressed by the addition of acetylsalicylate or of dinitrophenol.

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.

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