Acta Neuropathologica

, Volume 39, Issue 3, pp 219–223 | Cite as

δ-Aminolaevulinic acid dehydratase activity and focal brain haemorrhages in lead-treated rats

  • J. J. Barlow
  • J. K. Baruah
  • A. N. Davison
Original Investigations


Mothers were fed a diet containing 2% lead acetate according to the Pentschew-Garro model for inducing lead encephalopathy in young rats. At 20–22 days of age the young lead-treated rats had a mean brain Pb of 2.8 μg/g and liver Pb of 11 μg/g. The ALA dehydratase activity decreased 29% in brain and 69% in liver compared to controls, suggesting that the enzyme activity is related to the tissue lead level.

Mothers that had received lead prior to conception gave birth to pups with a significantly raised mean blood lead level (44 μg%). The ALA dehydratase activity in brain and liver was unchanged, suggesting that low blood lead levels may be insufficient to inhibit this enzyme in the rat. Focal haemorrhages were present, however, in the cerebral cortex of some of the pups from the lead-treated mothers. It is concluded that damage to the rat brain vascular system is a better index of lead toxicity than measurement of the lead sensitive enzyme ALA dehydratase.

Key words

Lead δ-Aminolaevulinic acid dehydratase Rat brain Haemorrhage 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Barltrop, D.: Transfer of lead to the human fetus. In: Mineral metabolism in pediatrics, pp. 135–151 (eds. D. Barltrop, W. L. Barland). Philadelphia: Davis 1969Google Scholar
  2. Barlow, J. J., Davison, A. N.: δ-Aminolaevulinic acid dehydratase in rat and guinea-pig models of lead encephalopathy (in preparation)Google Scholar
  3. Bouldin, T. W., Krigman, M. R.: Acute lead encephalopathy in the guinea pig. Acta neuropath. (Berl.)33, 185–190 (1975)Google Scholar
  4. Delves, H. T.: A micro-sampling method for the rapid determination of lead in blood by atomic-absorption spectrophotometry. Analyst95, 431–438 (1970)Google Scholar
  5. Gibson, K. D., Neuberger, A., Scott, J. J.: The purification and properties of δ-aminolaevulinic acid dehydratase. Biochem. J.61, 618–629 (1955)Google Scholar
  6. Goldstein, G. W., Asbury, A. K., Diamond, I.: Pathogenesis of lead encephalopathy. Arch. Neurol.31, 382–389 (1974)Google Scholar
  7. Goyer, R. A., Rhyne, B. C.: Pathological effects of lead. Int. Rev. Exp. Pathol.12, 1–77 (1973)Google Scholar
  8. Hernberg, S., Nikkanen, J.: Enzyme inhibition by lead under normal urban conditions. LancetI, 63–64 (1976)Google Scholar
  9. Hernberg, S. E., Nikkanen, J., Mellin, G.: δ-Aminolaevulinic acid dehydratase as a measure of lead exposure. Arch. Environ. Health (Chicago)21, 140–145 (1970)Google Scholar
  10. Krigman, M. R., Druse, M. J., Traylor, T. D., Wilson, M. H., Newell, B. S., Hogan, E. L.: Lead encephalopathy in the developing rat: Effect upon myelination. J. Neuropath. exp. Neurol.33, 58–73 (1974a)Google Scholar
  11. Krigman, M. R., Druse, M. J., Traylor, J. D., Wilson, M. H., Newell, B. S., Hogan, E. L.: Lead encephalopathy in the developing rat: Effect on cortical ontogenesis. J. Neuropath. exp. Neurol.33, 671–686 (1974b)Google Scholar
  12. Mauzerall, D., Granick, S.: The occurrence and determination of δ-aminolaevulinic acid and porphobilinogen in urine. J. biol. Chem.219, 435–446 (1956)Google Scholar
  13. Michaelson, I. A., Sauerhoff, M. W.: Animal models of human disease: Severe and mild lead encephalopathy in the neonatal rat. In: Environmental health perspectives, pp. 187–225, No. 7, 1974Google Scholar
  14. Millar, J. A., Battistini, V., Cumming, R. L. C., Carswell, F., Goldberg, A.: Lead and δ-aminolaevulinic acid dehydratase levels in mentally retarded children and in lead-poisoned suckling rats. LancetII, 695–698 (1970)Google Scholar
  15. Patel, A. J., Michaelson, I. A., Cremer, J. E., Balazs, R.: The metabolism of [14C]glucose by the brains of suckling rats intoxicated with inorganic lead. J. Neurochem.22, 581–590 (1974a)Google Scholar
  16. Patel, A. J., Michaelson, I. A., Cremer, J. E., Balasz, R.: Changes within metabolic compartments in the brains of young rats ingesting lead. J. Neurochem.22, 591–598 (1974b)Google Scholar
  17. Pentschew, A., Garro, F.: Lead encephalomyelopathy of the suckling rat and its implications on the porphyrinopathic nervous diseases. Acta neuropath.6, 266–278 (1966)Google Scholar
  18. Press, M. F.: Lead encephalopathy in neonatal Long-Evans rats: Morphological studies. J. Neuropath., exp. Neurol.36, 169–193 (1977)Google Scholar
  19. Weissberg, J. B., Lipschutz, F., Oski, F. A.: A sensitive laboratory test for the detection of childhood lead poisoning. New Engl. J. Med.284, 565–569 (1971)Google Scholar
  20. Weller, C. V.: Tolerance in respect to the meningo-cerebral manifestations of acute and sub-acute lead poisoning. Arch. intern. Med.39, 45–59 (1927)Google Scholar

Copyright information

© Springer-Verlag 1977

Authors and Affiliations

  • J. J. Barlow
    • 1
  • J. K. Baruah
    • 1
  • A. N. Davison
    • 1
  1. 1.Department of NeurochemistryInstitute of NeurologyLondonUK

Personalised recommendations