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Glucose-6-phosphate dehydrogenase deficiency and psychoses

  • A. Bocchetta
  • M. Del Zompo
  • G. U. Corsini

Abstract

Glucose-6-phosphate-dehydrogenase (G6PD) catalyzes the first step in the hexose monophosphate (HMP) shunt. This pathway serves to supply the cell with NADPH, the most important function being probably the maintainance of glutathione (GSH) in the reduced state. G6PD deficiency is the most common disease-producing enzyme deficiency of human beings, affecting about one hundred million people throughout the world. G6PD is subject to different mutations, and more than two hundred variants have been reported. Some of these cause a deficiency of enzyme activity in erythrocytes, leading to hemolitic anemia, usually upon exposure to an offending drug or toxin. Hemolysis may also occur during infection, diabetic acidosis, or when there is no known inciting cause. Some persons, perhaps carrying an additional genetic defect, show a particular sensitivity to fava beans (favism), whether upon ingestion or exposure to pollen. Different genetic variants of G6PD may have effects in tissues other than the erythrocytes, including the CNS.

Keywords

G6PD Deficiency Dehydrogenase Deficiency Color Blindness G6PD Activity Bipolar Illness 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Dern, RJ, Glynn, MF and Brewer, GJ (1962). Studies on the influence of hereditary G6PD deficiency in the expression of schizophrenic patterns. Clin Res, 10, 80Google Scholar
  2. 2.
    Dern, RJ, Glynn, MF and Brewer, GJ (1963). Studies on the correlation of the genetically determined trait, glucose-6-phosphate dehydrogenase deficiency, with behavioral manifestations in schizophrenia. J Lab Clin Med, 62, 319PubMedGoogle Scholar
  3. 3.
    Bowman, JE, Brewer, GJ, Frischer, H, Carter, JL, Eisenstein, RB and Bayrakci, C (1965). A re-evaluation of the relationship between glucose-6-phosphate dehydrogenase deficiency and the behavioral manifestations of schizophrenia. J Lab Clin Med, 65, 222PubMedGoogle Scholar
  4. 4.
    Fieve, RR, Brauninger, G, Fleiss, J and Cohen, G (1965). Glucose-6-phosphate dehydrogenase deficiency and schizophrenic behavior. J Psychiat Res, 3, 255PubMedCrossRefGoogle Scholar
  5. 5.
    Nasr, SJ (1976). Glucose-6-phosphate dehydrogenase deficiency with psychosis. Arch Gen Psychiat, 33, 1202PubMedGoogle Scholar
  6. 6.
    Nasr, SJ, Altman, E, Pscheidt, G and Meltzer, HY (1982). Glucose-6-phosphate dehydrogenase deficiency in a psychiatric population: a preliminary study. Biol Psychiatr, 17, 925Google Scholar
  7. 7.
    Bocchetta, A, Del Zompo M, Martis, G and Corsini, GU (1985). Glucose-6-phosphate dehydrogenase deficiency in a Sardinian psychiatric population. IVth World Congress of Biological Psychiatry, abs. 231. 1, p. 183Google Scholar
  8. 8.
    Spitzer, RL, Endicott, J and Robins, E (1977). Research Diagnostic Criteria, 3rd edition. ( New York: Biometric Research, New York State Psychiatric Institute )Google Scholar
  9. 9.
    Kornberg, A and Horecker, BL (1955). Glucose-6-phosphate de- hydrogenase. In: Colowick, SP and Kaplan, NO (eds.) “Methods in Enzymology”. p. 323. ( New York: Academic Press )CrossRefGoogle Scholar
  10. 10.
    Löhr, GW and Waller, HD (1974). Glucose-6-phosphate dehydrogenase. In: Bergmeyer, HU (ed.) “Methods of Enzymatic Analysis”. p. 636. ( New York: Academic Press )Google Scholar
  11. 11.
    Siniscalco, M, Bernini, L, Filippi, G, Latte, B, Meera Khan, P, Piomelli, S and Rattazzi, M (1966). Population genetics of haemoglobin variants, thalassaemia and glucose-6-phosphate dehydrogenase deficiency, with particular reference to the malaria hypothesis. Bull WHO, 34, 379PubMedGoogle Scholar
  12. 12.
    Meijer, A (1984). Psychiatric problems of children with glucose -6-phosphate dehydrogenase deficiency. Int J Psychiatr Med, 14, 207CrossRefGoogle Scholar
  13. 13.
    Gaetani, G, Salvidio, E, Pannacciulli, I, Ajmar, F and Paravidino, G (1970). Absence of haemolytic effects of L-Dopa on transfused G6PD-deficient erythrocytes. Experientia, 26, 785PubMedCrossRefGoogle Scholar
  14. 14.
    Goodwin, FK, Murphy, DL, Brodie, HKH and Bunney, WE (1971). Levodopa: alterations in behavior. Clin Pharmacol Ther, 12, 383PubMedGoogle Scholar
  15. 15.
    Mendlewicz, J, Yahr, F and Yahr, MD (1976). Psychiatric disorders in Parkinson’s disease treated with L-dopa: a genetic study. In: Birkmayer, W and Hornykiewicz, 0 (eds.) “Advances in Parkinson-ism”. p. 103. ( Basle: Editiones “Roche” )Google Scholar
  16. 16.
    Hothersall, JS, Greenbaum, AL and McLean, P (1982). The functional significance of the pentose phosphate pathway in synaptosomes: protection against peroxidative damage by catecholamines and oxidants. J Neurochem, 39, 1325PubMedCrossRefGoogle Scholar
  17. 17.
    Tabakoff, B, Groskopf, W, Anderson, R and Alivisatos, SGA (1974). Biogenic aldehyde metabolism, relation to pentose shunt activity in brain. Biochem Pharmacol, 23, 1707PubMedCrossRefGoogle Scholar
  18. 18.
    Maker, HS, Weiss, C, Silides, DJ and Cohen, G (1981). Coupling of dopamine oxidation (monoamine oxidase activity) to glutathione oxidation via the generation of hydrogen peroxide in rat brain homogenates. J Neurochem, 36, 589PubMedCrossRefGoogle Scholar
  19. 19.
    Engel, GL, Romano, J and Ferris, EB (1947). Effect of quinacrine (atabrine) on the central nervous system. Clinical and electroencephalografic studies. Arch Neurol Psychiat, 58, 337PubMedGoogle Scholar
  20. 20.
    Tarantino, LM and Hotta, SS (1974). Quinacrine stimulation of glutathione reduction dependent on the presence of a particulate brain subfraction. Proc Soc Exp Biol Med, 147, 887PubMedGoogle Scholar
  21. 21.
    Risch, N and Baron, M (1982). X-linkage and genetic heterogeneity in bipolar-related major affective illness: reanalysis of linkage data. Ann Hum Genet, 46, 153PubMedCrossRefGoogle Scholar
  22. 22.
    Thomson, G and Bodmer, W (1977). The genetic analysis of HLA and disease associations. In: Dausset, J and Svejgaard, A (eds.) “HLA and Disease”. p. 84. ( Copenhagen: Munksgaard )Google Scholar
  23. 23.
    Hodge, SE and Spence, MA (1981). Some epistatic two-locus models of disease. II. The confounding of linkage and association. Am J Hum Gen, 33, 396Google Scholar
  24. 24.
    Risch, N (1983). A general model for disease-marker association. Ann Hum Gen, 47, 245CrossRefGoogle Scholar
  25. 25.
    Mendlewicz, J, Linkowski, P and Willmotte, J (1980). Linkage between glucose-6-phosphate dehydrogenase deficiency and manic-depressive psychosis. Br J Psychiat, 137, 337CrossRefGoogle Scholar
  26. 26.
    Del Zompo, M, Bocchetta, A, Goldin, LR and Corsini, GU (1984). Linkage between X-chromosome markers and manic-depressive ilness. Acta Psychiatr Scand, 70, 282PubMedCrossRefGoogle Scholar
  27. 27.
    Baron, M, Risch, N, Hamburger, R, Mandel, B, Kushner, S, Newman, M, Drumer, D and Belmaker, RH (1987). Genetic linkage between X-chromosome markers and bipolar affective illness. Nature, 326, 289PubMedCrossRefGoogle Scholar
  28. 28.
    Risch, N,Baron, M and Mendlewicz, J (1986). Assessing the role of X-linked inheritance in bipolar-related major affective disorder. J Psychiatr Res, 20, 275PubMedCrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1990

Authors and Affiliations

  • A. Bocchetta
  • M. Del Zompo
  • G. U. Corsini

There are no affiliations available

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