Biography:

One of their most recent publications is Tissue slice respiration in the absence of suspension medium☆. Which was published in journal Archives of Biochemistry and Biophysics.

More information about E.A. Hosein research including statistics on their citations can be found on their Copernicus Academic profile page.

E.A. Hosein's Articles: (21)

Tissue slice respiration in the absence of suspension medium☆

AbstractSimple modifications made to the conventional Warburg respirometer enable the measurement of tissue slice respiration without medium. The tissue slice was layered on a platinum grid and respiration was measured in the usual manner. It was observed that the rate of tissue respiration is well maintained for 30 min. This method also permits measurement of the respiration of tissue slices obtained from animals previously treated with various drugs. Brain cortex slices from rats narcotized with Nembutal respired at rates similar to those found for normals, while slices from animals convulsed with dieldrin respired at a slower rate. Slices from animals poisoned either by cyanide or by azide respired at a faster rate, being between 30 and 45% higher than normals. The increased rate of respiration in these instances appeared to be due to increased lactate oxidation. The method described permits studies on the influence of pharmacologically active concentrations of drugs in vivo on in vitro respiration, without dilution effects while the drug is still within the tissue slice.

The isolation of γ-butyrobetaine, crotonbetaine and carnitine from brains of animals killed during induced convulsions☆

AbstractA mixture of γ-butyrobetaine, crotonbetaine, and carnitine was found to be present in aqueous extracts prepared from the brains of animals killed during convulsions caused by the administration of central nervous system stimulant drugs and by electroshock. Evidence contributing to the identification of these substances was obtained from Reinecke salt precipitation in acid, paper chromatographic analysis in two systems, and the melting points and mixed melting points of the chloroaurate derivatives. No such material could be found in similar extracts prepared from the brains of normal animals, animals convulsed with strychnine, nor from animals treated with central nervous system stimulant drugs but which were killed before convulsions occurred.

Acetylcholine-like activity in subcellular particles isolated from rat brain

AbstractBrain homogenates were separated into various subcellular fractions, and extracts of each fraction were further separated chromatographically with water-saturated butanol. Specific bands from the chromatograms were examined spectrophotometrically before biological assay for acetylcholine-like activity was performed. It was observed that the crude mitochondrial fraction contained most of the acetylcholine-like activity in the original homogenate. Further treatment of this fraction by differential centrifugation in sucrose solutions of varying densities showed that the subfraction presumed to contain presynaptic vesicles had most of the acetylcholine-like activity. In both sets of experiments the acetylcholine-like activity was mainly contributed by material which, in other work, was identified as a mixture of the CoA ester derivatives of γ-butyrobetaine, crotonbetaine, 1-carnitine, and acetyl-1-carnitine.

Biosynthesis of acetyl-l-carnityl choline

AbstractEarlier work had shown that acetyl-1-carnityl CoA was the material with acetylcholine-like activity which accumulated in the brain of narcotized rats. Accordingly, it was of importance to determine what normal function this material could have in the body. It appeared likely to be involved in acetylcholine and/or acetyl-1-carnityl choline formation. Since both these products are choline esters and it has been shown that the enzyme choline acetyltransferase is nonspecific for the esterification of choline, we have used the acetyl-1-carnityl CoA from narcotized brain extracts to determine which of these two products is produced when this substance is reacted with an extract of rat brain acetone powder as source of enzyme and choline. It was found that acetyl-1-carnityl choline could have been the only product formed under the particular reaction conditions studied. Product formation was indicated by increased acetylcholine-like activity as determined by bioassay. Acetylcholine formation could not be demonstrated with the particular reaction studied. These results also provide further evidence that the material with acetylcholine-like activity present in brain extracts from narcotized rats was not acetylcholine.

The influence of chronic ethanol feeding to rats on the integrity of liver mitochondrial membrane as assessed with the Mg2+-stimulated ATPase enzyme

AbstractIn using Mg2+-stimulated ATPase as an indicator for mitochondrial membrane damage, many authors in the past have done so by assaying at a single temperature. This has led us to make a comparison of this enzyme in two mitochondrial preparations using substrate concentrations which give near V activity. Results obtained with this enzyme using different temperature and substrate concentrations show that ethanol treatment to rats had indeed affected both the activity of this enzyme and the liver inner mitochondrial membrane. This is evidenced by the appearance of a phase-transition temperature at 32 °C in Arrhenius plots of samples from the alcoholic liver but not the controls. It was observed that when the assay was carried out below 26 °C, mitochondria from rats treated chronically with ethanol had diminished ATPase activity. In addition, it was observed that, in mitochondrial ghosts, chronic ethanol feeding caused a decrease in the phase-transition temperature observed in Arrhenius plots, usually associated with the lipid phase transition, from the normal value of 18.5 ± 0.2 to 15.8 ± 0.3 °C in the alcoholic. A similar decrease in phase-transition temperature was also obtained with sonicated liver mitochondrial membrane preparations from chronically ethanol-fed rats when compared to chow-fed control rats. Throughout the entire range of temperatures used in the assay, it was observed that the activation energies of the control and chronic alcoholic mitochondrial preparations were different. These results affirm that chronic ethanol treatment alters the liver mitochondrial membrane structure or enzyme microenvironment, which in turn may affect mitochondrial function.

Monitoring the stereospecificity of morphine action in vivo and in vitro through brain membrane lipid fluidity

AbstractDifferential scanning calorimetry of crude brain mitochondrial lipids obtained from control and morphine treated rats was carried out and the lipid phase transition measured. Morphine treatment resulted in a significant decrease in the temperature range and enthalpy of the phase transition. This effect was found to be dose dependent and reversible both in vivo and in vitro by naloxone. Studies with levorphanol and dextrorphan demonstrated stereospecificity. Furthermore, the ether precipitable fraction of total lipid extracts was shown to mediate the opiate response.

Tissue slice respiration in the absence of suspension medium☆

AbstractSimple modifications made to the conventional Warburg respirometer enable the measurement of tissue slice respiration without medium. The tissue slice was layered on a platinum grid and respiration was measured in the usual manner. It was observed that the rate of tissue respiration is well maintained for 30 min. This method also permits measurement of the respiration of tissue slices obtained from animals previously treated with various drugs. Brain cortex slices from rats narcotized with Nembutal respired at rates similar to those found for normals, while slices from animals convulsed with dieldrin respired at a slower rate. Slices from animals poisoned either by cyanide or by azide respired at a faster rate, being between 30 and 45% higher than normals. The increased rate of respiration in these instances appeared to be due to increased lactate oxidation. The method described permits studies on the influence of pharmacologically active concentrations of drugs in vivo on in vitro respiration, without dilution effects while the drug is still within the tissue slice.

The isolation of γ-butyrobetaine, crotonbetaine and carnitine from brains of animals killed during induced convulsions☆

AbstractA mixture of γ-butyrobetaine, crotonbetaine, and carnitine was found to be present in aqueous extracts prepared from the brains of animals killed during convulsions caused by the administration of central nervous system stimulant drugs and by electroshock. Evidence contributing to the identification of these substances was obtained from Reinecke salt precipitation in acid, paper chromatographic analysis in two systems, and the melting points and mixed melting points of the chloroaurate derivatives. No such material could be found in similar extracts prepared from the brains of normal animals, animals convulsed with strychnine, nor from animals treated with central nervous system stimulant drugs but which were killed before convulsions occurred.

Acetylcholine-like activity in subcellular particles isolated from rat brain

AbstractBrain homogenates were separated into various subcellular fractions, and extracts of each fraction were further separated chromatographically with water-saturated butanol. Specific bands from the chromatograms were examined spectrophotometrically before biological assay for acetylcholine-like activity was performed. It was observed that the crude mitochondrial fraction contained most of the acetylcholine-like activity in the original homogenate. Further treatment of this fraction by differential centrifugation in sucrose solutions of varying densities showed that the subfraction presumed to contain presynaptic vesicles had most of the acetylcholine-like activity. In both sets of experiments the acetylcholine-like activity was mainly contributed by material which, in other work, was identified as a mixture of the CoA ester derivatives of γ-butyrobetaine, crotonbetaine, 1-carnitine, and acetyl-1-carnitine.

Biosynthesis of acetyl-l-carnityl choline

AbstractEarlier work had shown that acetyl-1-carnityl CoA was the material with acetylcholine-like activity which accumulated in the brain of narcotized rats. Accordingly, it was of importance to determine what normal function this material could have in the body. It appeared likely to be involved in acetylcholine and/or acetyl-1-carnityl choline formation. Since both these products are choline esters and it has been shown that the enzyme choline acetyltransferase is nonspecific for the esterification of choline, we have used the acetyl-1-carnityl CoA from narcotized brain extracts to determine which of these two products is produced when this substance is reacted with an extract of rat brain acetone powder as source of enzyme and choline. It was found that acetyl-1-carnityl choline could have been the only product formed under the particular reaction conditions studied. Product formation was indicated by increased acetylcholine-like activity as determined by bioassay. Acetylcholine formation could not be demonstrated with the particular reaction studied. These results also provide further evidence that the material with acetylcholine-like activity present in brain extracts from narcotized rats was not acetylcholine.

The influence of chronic ethanol feeding to rats on the integrity of liver mitochondrial membrane as assessed with the Mg2+-stimulated ATPase enzyme

AbstractIn using Mg2+-stimulated ATPase as an indicator for mitochondrial membrane damage, many authors in the past have done so by assaying at a single temperature. This has led us to make a comparison of this enzyme in two mitochondrial preparations using substrate concentrations which give near V activity. Results obtained with this enzyme using different temperature and substrate concentrations show that ethanol treatment to rats had indeed affected both the activity of this enzyme and the liver inner mitochondrial membrane. This is evidenced by the appearance of a phase-transition temperature at 32 °C in Arrhenius plots of samples from the alcoholic liver but not the controls. It was observed that when the assay was carried out below 26 °C, mitochondria from rats treated chronically with ethanol had diminished ATPase activity. In addition, it was observed that, in mitochondrial ghosts, chronic ethanol feeding caused a decrease in the phase-transition temperature observed in Arrhenius plots, usually associated with the lipid phase transition, from the normal value of 18.5 ± 0.2 to 15.8 ± 0.3 °C in the alcoholic. A similar decrease in phase-transition temperature was also obtained with sonicated liver mitochondrial membrane preparations from chronically ethanol-fed rats when compared to chow-fed control rats. Throughout the entire range of temperatures used in the assay, it was observed that the activation energies of the control and chronic alcoholic mitochondrial preparations were different. These results affirm that chronic ethanol treatment alters the liver mitochondrial membrane structure or enzyme microenvironment, which in turn may affect mitochondrial function.

Tissue slice respiration in the absence of suspension medium☆

AbstractSimple modifications made to the conventional Warburg respirometer enable the measurement of tissue slice respiration without medium. The tissue slice was layered on a platinum grid and respiration was measured in the usual manner. It was observed that the rate of tissue respiration is well maintained for 30 min. This method also permits measurement of the respiration of tissue slices obtained from animals previously treated with various drugs. Brain cortex slices from rats narcotized with Nembutal respired at rates similar to those found for normals, while slices from animals convulsed with dieldrin respired at a slower rate. Slices from animals poisoned either by cyanide or by azide respired at a faster rate, being between 30 and 45% higher than normals. The increased rate of respiration in these instances appeared to be due to increased lactate oxidation. The method described permits studies on the influence of pharmacologically active concentrations of drugs in vivo on in vitro respiration, without dilution effects while the drug is still within the tissue slice.

The isolation of γ-butyrobetaine, crotonbetaine and carnitine from brains of animals killed during induced convulsions☆

AbstractA mixture of γ-butyrobetaine, crotonbetaine, and carnitine was found to be present in aqueous extracts prepared from the brains of animals killed during convulsions caused by the administration of central nervous system stimulant drugs and by electroshock. Evidence contributing to the identification of these substances was obtained from Reinecke salt precipitation in acid, paper chromatographic analysis in two systems, and the melting points and mixed melting points of the chloroaurate derivatives. No such material could be found in similar extracts prepared from the brains of normal animals, animals convulsed with strychnine, nor from animals treated with central nervous system stimulant drugs but which were killed before convulsions occurred.

Acetylcholine-like activity in subcellular particles isolated from rat brain

AbstractBrain homogenates were separated into various subcellular fractions, and extracts of each fraction were further separated chromatographically with water-saturated butanol. Specific bands from the chromatograms were examined spectrophotometrically before biological assay for acetylcholine-like activity was performed. It was observed that the crude mitochondrial fraction contained most of the acetylcholine-like activity in the original homogenate. Further treatment of this fraction by differential centrifugation in sucrose solutions of varying densities showed that the subfraction presumed to contain presynaptic vesicles had most of the acetylcholine-like activity. In both sets of experiments the acetylcholine-like activity was mainly contributed by material which, in other work, was identified as a mixture of the CoA ester derivatives of γ-butyrobetaine, crotonbetaine, 1-carnitine, and acetyl-1-carnitine.

Biosynthesis of acetyl-l-carnityl choline

AbstractEarlier work had shown that acetyl-1-carnityl CoA was the material with acetylcholine-like activity which accumulated in the brain of narcotized rats. Accordingly, it was of importance to determine what normal function this material could have in the body. It appeared likely to be involved in acetylcholine and/or acetyl-1-carnityl choline formation. Since both these products are choline esters and it has been shown that the enzyme choline acetyltransferase is nonspecific for the esterification of choline, we have used the acetyl-1-carnityl CoA from narcotized brain extracts to determine which of these two products is produced when this substance is reacted with an extract of rat brain acetone powder as source of enzyme and choline. It was found that acetyl-1-carnityl choline could have been the only product formed under the particular reaction conditions studied. Product formation was indicated by increased acetylcholine-like activity as determined by bioassay. Acetylcholine formation could not be demonstrated with the particular reaction studied. These results also provide further evidence that the material with acetylcholine-like activity present in brain extracts from narcotized rats was not acetylcholine.

Tissue slice respiration in the absence of suspension medium☆

AbstractSimple modifications made to the conventional Warburg respirometer enable the measurement of tissue slice respiration without medium. The tissue slice was layered on a platinum grid and respiration was measured in the usual manner. It was observed that the rate of tissue respiration is well maintained for 30 min. This method also permits measurement of the respiration of tissue slices obtained from animals previously treated with various drugs. Brain cortex slices from rats narcotized with Nembutal respired at rates similar to those found for normals, while slices from animals convulsed with dieldrin respired at a slower rate. Slices from animals poisoned either by cyanide or by azide respired at a faster rate, being between 30 and 45% higher than normals. The increased rate of respiration in these instances appeared to be due to increased lactate oxidation. The method described permits studies on the influence of pharmacologically active concentrations of drugs in vivo on in vitro respiration, without dilution effects while the drug is still within the tissue slice.

The isolation of γ-butyrobetaine, crotonbetaine and carnitine from brains of animals killed during induced convulsions☆

AbstractA mixture of γ-butyrobetaine, crotonbetaine, and carnitine was found to be present in aqueous extracts prepared from the brains of animals killed during convulsions caused by the administration of central nervous system stimulant drugs and by electroshock. Evidence contributing to the identification of these substances was obtained from Reinecke salt precipitation in acid, paper chromatographic analysis in two systems, and the melting points and mixed melting points of the chloroaurate derivatives. No such material could be found in similar extracts prepared from the brains of normal animals, animals convulsed with strychnine, nor from animals treated with central nervous system stimulant drugs but which were killed before convulsions occurred.

Acetylcholine-like activity in subcellular particles isolated from rat brain

AbstractBrain homogenates were separated into various subcellular fractions, and extracts of each fraction were further separated chromatographically with water-saturated butanol. Specific bands from the chromatograms were examined spectrophotometrically before biological assay for acetylcholine-like activity was performed. It was observed that the crude mitochondrial fraction contained most of the acetylcholine-like activity in the original homogenate. Further treatment of this fraction by differential centrifugation in sucrose solutions of varying densities showed that the subfraction presumed to contain presynaptic vesicles had most of the acetylcholine-like activity. In both sets of experiments the acetylcholine-like activity was mainly contributed by material which, in other work, was identified as a mixture of the CoA ester derivatives of γ-butyrobetaine, crotonbetaine, 1-carnitine, and acetyl-1-carnitine.

Biosynthesis of acetyl-l-carnityl choline

AbstractEarlier work had shown that acetyl-1-carnityl CoA was the material with acetylcholine-like activity which accumulated in the brain of narcotized rats. Accordingly, it was of importance to determine what normal function this material could have in the body. It appeared likely to be involved in acetylcholine and/or acetyl-1-carnityl choline formation. Since both these products are choline esters and it has been shown that the enzyme choline acetyltransferase is nonspecific for the esterification of choline, we have used the acetyl-1-carnityl CoA from narcotized brain extracts to determine which of these two products is produced when this substance is reacted with an extract of rat brain acetone powder as source of enzyme and choline. It was found that acetyl-1-carnityl choline could have been the only product formed under the particular reaction conditions studied. Product formation was indicated by increased acetylcholine-like activity as determined by bioassay. Acetylcholine formation could not be demonstrated with the particular reaction studied. These results also provide further evidence that the material with acetylcholine-like activity present in brain extracts from narcotized rats was not acetylcholine.

The influence of chronic ethanol feeding to rats on the integrity of liver mitochondrial membrane as assessed with the Mg2+-stimulated ATPase enzyme

AbstractIn using Mg2+-stimulated ATPase as an indicator for mitochondrial membrane damage, many authors in the past have done so by assaying at a single temperature. This has led us to make a comparison of this enzyme in two mitochondrial preparations using substrate concentrations which give near V activity. Results obtained with this enzyme using different temperature and substrate concentrations show that ethanol treatment to rats had indeed affected both the activity of this enzyme and the liver inner mitochondrial membrane. This is evidenced by the appearance of a phase-transition temperature at 32 °C in Arrhenius plots of samples from the alcoholic liver but not the controls. It was observed that when the assay was carried out below 26 °C, mitochondria from rats treated chronically with ethanol had diminished ATPase activity. In addition, it was observed that, in mitochondrial ghosts, chronic ethanol feeding caused a decrease in the phase-transition temperature observed in Arrhenius plots, usually associated with the lipid phase transition, from the normal value of 18.5 ± 0.2 to 15.8 ± 0.3 °C in the alcoholic. A similar decrease in phase-transition temperature was also obtained with sonicated liver mitochondrial membrane preparations from chronically ethanol-fed rats when compared to chow-fed control rats. Throughout the entire range of temperatures used in the assay, it was observed that the activation energies of the control and chronic alcoholic mitochondrial preparations were different. These results affirm that chronic ethanol treatment alters the liver mitochondrial membrane structure or enzyme microenvironment, which in turn may affect mitochondrial function.

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