Influence of iron deficiency and lead treatment on behavior and cerebellar and hippocampal polyamine levels in neonatal rats
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Effect of lead exposure and iron-deficiency on polyamine levels in neuronal and glial cells of cerebellum and hippocampus was investigated in weaned rats. Lactating dams with one day old litters were given 0.2% (w/v) lead acetate in drinking water from postnatal day one to twenty one and maintained on an iron-deficient diet. There was an overall reduction of putrescine, spermidine and spermine in neuronal and glial cells of cerebellum and hippocampus consequent to lead exposure and iron-deficiency alone. Lead exposure and iron-deficiency together did not potentiate the polyamine levels in neuronal and glial cells of cerebellum and hippocampus uniformly. However, the enhanced lowering of putrescine in the hippocampal glia, spermidine in cerebellar neuronal and spermine in both neuronal and glial cells of cerebellum during the critical stage of brain development may result in stunted neuronal growth and sprouting in lead exposed and iron-deficient animals. The behavioral alterations as observed in the present study may be due to impaired neuronal development resulting from a depressed polyamine pathway and which could be attributed to cognitive deficits in growing children.
Key WordsIron-deficiency lead polyamines neuronal glial
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- 2.Legare, M. E., Castiglioni, A. J., Rowles, T. K., Calvin, J. A., Snydr-Armstead, C., and Tiffany Castiglioni, E. 1993. Morphological alterations of neurons and astrocytes in guinea pigs exposed to low levels of inorganic lead. Neurotoxicol. 14:77–80.Google Scholar
- 3.Goldstein, G. W. 1990. Lead poisoning and brain cell function. Env. Hlth. Perspectives 89:91–94.Google Scholar
- 4.Pounds, J. G., and Cory-slechta, D. A. 1993. New dimensions of lead neurotoxicity: redefining mechanisms and effects. Neurotoxicol. 14:4–6.Google Scholar
- 5.Yehuda, S., and Youdim, M. B. H. 1989. Brain iron: a lesson from animal models. Am. J. Clin. Nutr. 56(Suppl.):618–625.Google Scholar
- 13.Bell, J. M., and Slotkin, T. A. 1986. Polyamines as intermediates in developmental neurotoxic events. Neurotoxicol. 7:147–160.Google Scholar
- 16.Miller, G. D., Massaro, T. F., and Massaro, J. E. 1990. Interaction between lead and essential elements: a review. Neurotoxicol. 11: 99–120.Google Scholar
- 23.Seiler, N., and Lamberty, V. 1975. Interaction between polyamines and nucleic acids: changes of polyamines and nucleic acids in developing rat brain. J. Neurochem. 24:1–16.Google Scholar
- 25.Zar, H. J. 1984. Multifactorial analysis of variance. Pages 244–251, in Zar, H. J. (ed.), Biostatistical Analysis, Prentice Hall, New Jersey.Google Scholar
- 29.Youdim, M. B. H. 1990. Developmental, neuropharmacological and biochemical aspects of iron-deficiency. Pages 83–133,in Dobbing, J. (ed.), Brain, Behavior and Iron-deficiency, Springer, New York.Google Scholar
- 30.Youdim, M. B. H., Ben-Shachar, D., and Riederer, P. 1989. Is Parkinson's disease a progressive siderosis of substantia nigra resulting in iron and melanin induced neurodegeneration? Acta Neurol. Scand. 26:47–54.Google Scholar
- 34.Hubbel, R. B., Mendel, K. B., and Wakeman, A. J. 1937. A new salt mixture for use in experimental diets. J. Nutr. 14:273–285.Google Scholar