OXIDIZED AND REDUCED GLUTATHIONE IN THE RAT BRAIN UNDER NORMOXIC AND HYPOXIC CONDITIONS

In order to test the proposition that hypoxia leads to a change in the concentration ratio of reduced (GSH) and oxidized (GSSG) glutathione in the brain, enzymatic, fluorometric assays were worked out for measuring GSH and GSSG. In lightly anaesthetized and immobilized rats. GSH concentrations in the cerebral cortex and the cerebellum were close to 2 μmol.g‐1 while a slightly lower concentration (approx 1.4μmol.g‐1) was found in the brain stem. In order to avoid artefactual oxidation of GSH during sample preparation for GSSG determination the tissue was extracted with trichloroacetic acid, following alkylation of SH groups with N‐ethylmaleimide. With these precautions GSSG concentrations were approx 0.7% of the corresponding GSH concentrations. However. the results indicated that the true GSSG concentrations may be even lower. During hypoxia there was neither a decrease in GSH nor an increase in GSSG concentrations in cortical tissue or cisternal CSF.

[1]  B. Chance,et al.  Properties of glutathione release observed during reduction of organic hydroperoxide, demethylation of aminopyrine and oxidation of some substances in perfused rat liver, and their implications for the physiological function of catalase. , 1977, The Biochemical journal.

[2]  M. Orłowski,et al.  Glutathione metabolism and some possible functions of glutathione in the nervous system. , 1976, International review of neurobiology.

[3]  B. Siesjö,et al.  Rate of energy utilization in the cerebral cortex of rats. , 1975, Acta physiologica Scandinavica.

[4]  B. Siesjö,et al.  Influence of complete ischemia on glycolytic metabolites, citric acid cycle intermediates, and associated amino acids in the rat cerebral cortex. , 1974, Brain research.

[5]  A. Meister.  Theγ-Glutamyl Cycle: Diseases Associated with Specific Enzyme Deficiencies , 1974 .

[6]  W. M. Hadley,et al.  Modified fluorescence assay for oxidized and reduced glutathione in tissue. , 1974, Journal of pharmaceutical sciences.

[7]  K. Domanska-Janik,et al.  Regulation of thiols in the brain. I. Concentrations of thiols and glutathione reductase activity in different parts of the rat brain during hypoxia. , 1974, Resuscitation.

[8]  K. Domanska-Janik,et al.  Regulation of thiols in the brain. 2. Effect of hypoxia on the activities of cytoplasmic NADPH-producing enzymes in different parts of the rat brain. , 1974, Resuscitation.

[9]  L. Salford,et al.  OPTIMAL FREEZING CONDITIONS FOR CEREBRAL METABOLITES IN RATS , 1973, Journal of neurochemistry.

[10]  F. Plum,et al.  Graded hypoxia-oligemia in rat brain. I. Biochemical alterations and their implications. , 1973, Archives of neurology.

[11]  B. Siesjö,et al.  THE EFFECT OF HYPERCAPNIC ACIDOSIS UPON SOME GLYCOLYTIC AND KREBS CYCLE‐ASSOCIATED INTERMEDIATES IN THE RAT BRAIN , 1972, Journal of neurochemistry.

[12]  B. Siesjö,et al.  THE EFFECT OF MODERATE AND MARKED HYPERCAPNIA UPON THE ENERGY STATE AND UPON THE CYTOPLASMIC NADH/NAD+ RATIO OF THE RAT BRAIN , 1972, Journal of neurochemistry.

[13]  L. Flohé,et al.  Oxidation in the NADP system and release of GSSG from hemoglobin‐free perfused rat liver during peroxidatic oxidation of glutathione by hydroperoxides , 1972, FEBS letters.

[14]  H. Krebs,et al.  The redox state of free nicotinamide-adenine dinucleotide phosphate in the cytoplasm of rat liver. , 1969, The Biochemical journal.

[15]  J. Visser,et al.  Purification and properties of glutathione reductase of human erythrocytes. , 1969, Biochimica et biophysica acta.

[16]  S. Srivastava,et al.  Cataract produced by tyrosinase and tyrosine systems in rabbitens in vitro. , 1969, The Biochemical journal.

[17]  S. Srivastava,et al.  The transport of oxidized glutathione from human erythrocytes. , 1969, The Journal of biological chemistry.

[18]  B. Christophersen.  Formation of monohydroxy-polyenic fatty acids from lipid peroxides by a glutathione peroxidase. , 1968, Biochimica et biophysica acta.

[19]  C. Little,et al.  An intracellular GSH-peroxidase with a lipid peroxide substrate. , 1968, Biochemical and biophysical research communications.

[20]  N. Haugaard.  Cellular mechanisms of oxygen toxicity. , 1968, Physiological reviews.

[21]  S. Srivastava,et al.  Accurate measurement of oxidized glutathione content of human, rabbit, and rat red blood cells and tissues. , 1968, Analytical biochemistry.

[22]  B. Christophersen.  The inhibitory effect of reduced glutathione on the lipid peroxidation of the microsomal fraction and mitochondria. , 1968, The Biochemical journal.

[23]  O. H. Lowry,et al.  Effects of changes in brain metabolism on the levels of citric acid cycle intermediates. , 1966, The Journal of biological chemistry.

[24]  H Güntherberg,et al.  The true oxidized glutathione content of red blood cells obtained by new enzymic and paper chromatographic methods. , 1966, Analytical biochemistry.

[25]  B. Siesjö,et al.  Gradients of CO2 tension in the brain. , 1966, Acta physiologica Scandinavica.

[26]  B. E. Davidson,et al.  The estimation of glutathione in rat tissues. A comparison of a new spectrophotometric method with the glyoxalase method. , 1964, The Biochemical journal.

[27]  S. Rapoport,et al.  Reduction-potential of Glutathione , 1964, Nature.

[28]  B. Siesjö.  The Solubility of Carbon Dioxide in Cerebral Cortical Tissue of Cats With a note on the solubility of carbon dioxide in water, 0.16 M NaCl and cerebrospinal fluid. , 1962 .

[29]  A. Pihl,et al.  CHAPTER 4 – Mechanisms of Protective and Sensitizing Action , 1960 .

[30]  G. Ellman,et al.  Tissue sulfhydryl groups. , 1959, Archives of biochemistry and biophysics.

[31]  H. Mcilwain,et al.  Glutathione, oxidized and reduced, in the brain and in isolated cerebral tissue. , 1959, The Biochemical journal.

[32]  Flexible System , 2022 .