Skip to main content
SpringerLink
Log in

Relation Between Free Fatty Acid and Acyl-CoA Concentrations in Rat Brain Following Decapitation

  • Published:
Neurochemical Research Aims and scope Submit manuscript

Abstract

To ascertain effects of total ischemia on brain phospholipid metabolism, anesthetized rats were decapitated and unesterified fatty acids and long chain acyl-CoA concentrations were analyzed in brain after 3 or 15 min. Control brain was taken from rats that were microwaved. Fatty acids were quantitated by extraction, thin layer chromatography and gas chromatography. Long-chain acyl-CoAs were quantitated by solubilization, solid phase extraction with an oligonucleotide purification cartridge and HPLC. Unesterified fatty acid concentrations increased significantly after decapitation, most dramatically for arachidonic acid (76 fold at 15 min) followed by docosahexaenoic acid. Of the acyl-CoA molecular species only the concentration of arachidonoyl-CoA was increased at 3 min and 15 min after decapitation, by 3–4 fold compared with microwaved brain. The concentration of docosahexaenoyl-CoA fell whereas concentrations of the other acyl-CoAs were unchanged. The increase in arachidonoyl-CoA after decapitation indicates that reincorporation of arachidonic acid into membrane phospholipids is possible during ischemia, likely at the expense of docosahexaenoic acid.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

REFERENCES

  1. Rapoport, S. I., Lust, W. D., and Fredericks, W. R. 1986. Effects of hypoxia on rat brain metabolism: unilateral in vivo carotid infusion. Exp. Neurobiol. 91, 319–330.

    Google Scholar 

  2. Farooqui, A. A., and Horrocks, L. A. 1991. Excitatory amino acid receptors, neural membrane phospholipid metabolism and neurological disorders. Brain Res. Rev. 16:171–191.

    Google Scholar 

  3. Siesjö, B. K. 1992. Pathophysiology and treatment of focal cerebral ischemia. J. Neurosurg. 77:169–184.

    Google Scholar 

  4. Choi, D. W. 1990. Methods for antagonizing glutamate neurotoxicity. Cerebrovascular and Brain Metabolism Rev. 2:105–147.

    Google Scholar 

  5. Birkle, D. L. 1992. Reciprocal regulation of fatty acid release in the brain by GABA and glutamate in Neurobiology of Essential Fatty Acids (Bazan N. G., ed.) pp. 57–71. Plenum Press, New York.

    Google Scholar 

  6. Bazan, N. G. 1970. Effects of ischemia and electroconvulsive shock on free fatty acid pool in the brain. Biochim. Biophys. Acta 218:1–10.

    Google Scholar 

  7. Bazan, N. G. 1976. Free arachidonic acid and other lipids in the nervous system during early ischemia and after electroshock, in Advances in Experimental Medicine and Biology, Vol. 72: Function and Metabolism of Phospholipids in the Central and Peripheral Nervous System (Porcellati G., Amaducci, L., and Galli, C., eds), pp. 317–335. Plenum Press, New York/London.

    Google Scholar 

  8. Sun, G. Y., Lu, F. L., Lin, S. E., and Ko, M. R. 1992. Decapitation ischemia-induced release of free fatty acids in mouse brain. Mol Cell Neuropathol. 17:39–50.

    Google Scholar 

  9. Reddy, T. S., and Bazan, N. G. 1987. Arachidonic acid, stearic acid, and diacylglycerol accumulation correlates with the loss of phosphatidylinositol 4,5-bisphosphate in cerebrum 2 seconds after electroconvulsive shock: complete reversion of changes 5 minutes after stimulation. J. Neurosci. Res. 18:449–455.

    Google Scholar 

  10. Ikeda, M., Yoshida, S., Busto, R., Santiso, M., and Ginsberg, M. D. 1986. Polyphosphoinositides as a probable source of brain free fatty acids accumulated at the onset of ischemia. J. Neurochem. 47:123–132.

    Google Scholar 

  11. Lee, C., and Hajra, A. K. 1991. Molecular species of diacylglycerols and phosphoglycerides and the postmortem changes in the molecular species of diacylglycerols in rat brains. J. Neurochem. 56:370–379.

    Google Scholar 

  12. Kumar, R., Harvey, S., Kester, N., Hanahan, D., and Olson, M. 1988. Production and effects of platelet-activating factor in the rat brain. Biochim. Biophys. Acta 963:375–383.

    Google Scholar 

  13. Birkle, D. L., Kurian, P., Braquet, P., and Bazan, N. G. 1988. Platelet-activating factor antagonist BN 52021 decreases accumulation of free polyunsaturated fatty acid in mouse brain during ischemia and electroconvulsive shock. J. Neurochem. 51:1900–1905.

    Google Scholar 

  14. Edgar, A. D., Strosznajder, J., and Horrocks, L. A. 1982. Activation of ethanolamine phospholipase A2 in brain during ischemia. J. Neurochem. 39:1111–1116.

    Google Scholar 

  15. MacDonald, J. I. S, and Sprecher, H. 1991. Phospholipid fatty acid remodeling in mammalian cells. Biochim. Biophys. Acta 1084:105–121.

    Google Scholar 

  16. Waku, K. 1992. Origins and fates of fatty acyl-CoA esters. Biochim. Biophys. Acta 1124:101–111.

    Google Scholar 

  17. Rehncrona, S., Westerberg, E., Akesson, B., and Siesjö, B. K. 1982. Brain cortical fatty acids and phospholipids during and following complete and severe incomplete ischemia. J. Neurochem. 38:84–93.

    Google Scholar 

  18. Yoshida, S., Ikeda, M., Busto, R., Santiso, M., Martinez, E., and Ginsberg, M. D. 1986. Cerebral phosphoinositide, triacylglycerol, and energy metabolism in reversible ischemia:origin and fate of free fatty acids. J. Neurochem. 47:744–757.

    Google Scholar 

  19. Ikeda, M., Busto, R., Yoshida, S., Santiso, M., Martinez, E., and Ginsberg, M. D. 1988. Cerebral phosphoinositide, triacylglycerol and energy metabolism during severe hypoxia and recovery. Brain Research 459:344–350.

    Google Scholar 

  20. Deutsch, J., Grange, E., Rapoport, S. I., and Purdon, A. D. 1994. Isolation and quantitation of acyl-CoA esters in brain tissue by solid phase extraction. Analytical Biochem. 220:321–23.

    Google Scholar 

  21. Okuyama, H., Lands, W. E. M., Christie, W. W., and Gunstone, F. D. 1969. Selective transfer of cyclopropane acids by acyl-coenzyme A:phospholipid acyltransferase. J. Biol. Chem. 244, 6514–6519.

    Google Scholar 

  22. Washizaki, K., Smith, Q. R., Rapoport, S. I., and Purdon, A. D. 1994. Brain arachidonic acid incorporation and precursor pool specific activity during intravenous infusion of unesterified [3H]arachidonate in the anesthetized rat J. Neurochem. 63:727–736.

    Google Scholar 

  23. Folch, J., Lees, M., and Stanley, G. H. S. 1957. A simple method for the isolation and purification of total lipides from animal tissues. J. Biol. Chem. 226, 497–509.

    Google Scholar 

  24. Begun, J. M. 1985. Newman-Keuls Procedure in Encyclopaedia of Statistical Sciences, pp 200–201.

  25. Robinson, P. J., Noronha, J., DeGeorge, J. J., Freed, L. M., Nariai, T., and Rapoport, S. I. 1992. A quantitative method for measuring regional in vivo fatty-acid incorporation into and turnover within brain phospholipids: review and critical analysis. Brain Res. Rev. 17:187–214.

    Google Scholar 

  26. Rosendal, J., and Knudsen, J. 1992. A fast and versatile method for extraction and quantitation of long-chain acyl-CoA esters from tissue:content of individual long-chain acyl-CoA esters in various tissues from fed rats. Analytical Biochem. 207:63–67.

    Google Scholar 

  27. Reddy, T. S., and Bazan, N. G. 1983. Kinetic properties of arachidonoyl-Coenzyme A synthetase in rat brain microsomes. Arch. Biochem. Biophys. 226:125–133.

    Google Scholar 

  28. Reddy, T. S., Sprecher, H., and Bazan, N. G. 1984. Long-chain acyl-coenzyme A synthetase from rat brain microsomes. Kinetic studies using [1 — 14C]docosahexaenoic acid substrate. Eur. J. Biochem. 145:21–29.

    Google Scholar 

  29. Laposata, M., Reich, E. L., and Majerus, P. W. 1985. Arachidonoyl-CoA Synthetase. Separation from nonspecific acyl-CoA synthetase and distribution in various cells and tissues. J. Biol. Chem. 260:11016–11020.

    Google Scholar 

  30. Mandings, S., Hummel, R., Rawn, S., Jensen, G., Andreison, P. H., Gregersen, N., Knudsen, J., and Kristiansen, K. 1992. Acyl-CoA binding protein/diazepam-binding inhibitor gene and pseudogenes. A typical housekeeping gene family. J. Mol Biol. 228: 1011–1022.

    Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, 20892

    S. I. Rapoport & A. David Purdon

  2. The Department of Pharmaceutical Chemistry, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel

    Joseph Deutsch

  3. The Department of Pharmaceutical Chemistry, School of Pharmacy, The Hebrew University of Jerusalem, Jerusalem, Israel

    A. David Purdon

Authors
  1. Joseph Deutsch
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. S. I. Rapoport
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. A. David Purdon
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to A. David Purdon.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Deutsch, J., Rapoport, S.I. & Purdon, A.D. Relation Between Free Fatty Acid and Acyl-CoA Concentrations in Rat Brain Following Decapitation. Neurochem Res 22, 759–765 (1997). https://doi.org/10.1023/A:1022030306359

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1023/A:1022030306359

Search

Navigation