Abstract

BackgroundThe mechanism of aluminum-induced neurotoxicity is not clear. The involvement of glutamate in the aluminium-induced neurocomplications has been suggested. Brain glutamate levels also found to be altered in protein malnutrition. Alterations in glutamate levels as well as glutamate-α-decarboxylase in different regions of rat brain has been reported in response to aluminum exposure. Thus the study of glutamate metabolising enzymes in different brain regions of rats maintained on either normal or restricted protein diet may be of importance for understanding the neurotoxicity properties of aluminium.ResultsDietary protein restrictions does not have an significant impact on regional aluminum content of the brain. The interaction of aluminum intoxication and protein restriction is significant in the thalamic area and the midbrain-hippocampal region in cases of glutamate oxaloacetate transaminase. In the case of gluatmate pyruvate transaminase, this interaction is significant only in thalamic area.ConclusionThe metabolism of amino acids, as indicated by activities of specific transaminases, of brain is altered in response to aluminum exposure. These alterations are region specific and are dependent on dietary protein intake or manipulation of the brain amino acid homeostasis.

Highlights

  • The mechanism of aluminum-induced neurotoxicity is not clear

  • We have shown that aluminum causes alteration in glutamate levels and glutamate α-decarboxylase activities of different brain regions [11]

  • Though there is significant amount of added components for treatment effects in all of the tested brain regions, Scheffe's F test for multiple comparisons showed that aluminum exposure significantly increased the aluminum content of cerebrum, thalamic area and midbrain-hippocampal region of normal protein group and thalamic area and midbrain-hippocampal region of rats maintained on low protein diet

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Summary

Introduction

The mechanism of aluminum-induced neurotoxicity is not clear. Alterations in glutamate levels as well as glutamate-α-decarboxylase in different regions of rat brain has been reported in response to aluminum exposure. The study of glutamate metabolising enzymes in different brain regions of rats maintained on either normal or restricted protein diet may be of importance for understanding the neurotoxicity properties of aluminium. The mechanism of aluminum-induced neurotoxicity is not clear [4,5]. There are suggestions that glutamate may be involved in the aluminum-induced neurocomplications. It has been reported that aluminum impairs the glutamatergic neurotransmission [8] and mediates glutamate-induced neurotoxicity in organotypic cultures [9]. We have shown that aluminum causes alteration in glutamate levels and glutamate α-decarboxylase activities of different brain regions [11]. We had shown dietary protein restrictions to alter the aluminum-

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