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Neurobehavioral, Neuroendocrine and Neurochemical Effects of Zinc Supplementation in Rats

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Excitatory Amino Acids and Epilepsy

Abstract

Extensive morphological and biochemical investigations have been devoted to the neurological effects induced by zinc deficiency since this trace metal has been recognized as essential during neurogenesis for a normal development of the central nervous system (for a review see Dreosti, 1984; Sandstead, 1984). Less attention, however, has been addressed to the neurological consequences of an increased supplementation of zinc.In this context it must be mentioned that the peripheral acute administration of zinc intravenously or intraperitoneally in doses up to 100 mg/kg has not been associated with the production of convulsive seizures or other behavioral abnormalities (Ebadi et al., 1984). From these results, it has been concluded that after parenteral acute administration, zinc does not induce any effect since: a) by binding to circulating proteins such as albumin, gamma-globulins and probably other proteins (Prasad, 1979; Disilvestro and Cousins, 1983; Ebadi et al., 1984) it is unavailable to the CNS; b) it exists mostly in bound form in the brain (Ebadi et al., 1984). In an attempt to gain more information on the behavioral effects induced by peripheral supplementation of zinc, we obtained the same results with regard to the lack of convulsions. In our experience, however, acute intraperitoneal injections of zinc sulphate or zinc acetate induced, in a dose-related fashion starting from 50 mg/kg, a sedative effect which caused a 50% mortality rate within six hours at 200 mg/kg. Based on physiological considerations and on our present observations, it seems more likely to suggest that zinc enters the brain but does not reach concentrations sufficient to induce epileptic seizures which can be elicited by its intracerebroventricular administration (Itoh and Ebadi, 1982; Ebadi et al., 1984). The levels of zinc tested in six brain areas of these rats did not show significant variation in comparison with controls, whereas zinc plasma levels were found to be increased. Time-course determinations of zinc in blood and brain areas are needed in order to explain these data. On the other hand, there are several question marks concerning the machinery which regulates zinc homeostasis in the brain. Thus, it is difficult to explain cerebral zinc uptake and turnover (Kasarskis, 1984) and the unaltered zinc levels in the brain of zinc deficient rats (Wallwork et al., 1983; Kasarskis, 1984) as well as the mechanisms which regulate the bound/free zinc ratio.

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© 1986 Plenum Press, New York

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Baraldi, M. et al. (1986). Neurobehavioral, Neuroendocrine and Neurochemical Effects of Zinc Supplementation in Rats. In: Schwarcz, R., Ben-Ari, Y. (eds) Excitatory Amino Acids and Epilepsy. Advances in Experimental Medicine and Biology, vol 203. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7971-3_44

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  • DOI: https://doi.org/10.1007/978-1-4684-7971-3_44

  • Publisher Name: Springer, Boston, MA

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