Dietary protein restriction causes modification in aluminum-induced alteration in glutamate and GABA system of rat brain

Abstract

Background: Alteration of glutamate and γ-aminobutyrate system have been reported to be associated with neurodegenerative disorders and have been postulated to be involved in aluminuminduced neurotoxicity as well. Aluminum, an well known and commonly exposed neurotoxin, was found to alter glutamate and γ-aminobutyrate levels as well as activities of associated enzymes with regional specificity. Protein malnutrition also reported to alter glutamate level and some of its metabolic enzymes. Thus the region-wise study of levels of brain glutamate and γ-aminobutyrate system in protein adequacy and inadequacy may be worthwhile to understand the mechanism of aluminum-induced neurotoxicity.

Structural features of aluminium(III) complexes with bioligands in glutamate dehydrogenase reaction system – A review

“…L-Glu is an important acidic neurotransmitter in the central nervous system. Alternated configuration of L-Glu has been reported to be associated with neurodegenerative disorders and has been postulated to be involved in aluminium-induced neurotoxicity as well [1]. The complexation of Al(III) with glutamate has been studied by Kiss group and the stability constants have been measured [21,22].…”

“…Aluminium, a well known and commonly exposed neurotoxin, was found to alter glutamate and c-aminobutyrate levels as well as activities of the associated enzymes with regional specificity [1]. Al(III) also inhibits glutamate dehydrogenase (GDH), a central enzyme in glutamate metabolism [2].…”

Does neurotransmission impairment accompany aluminium neurotoxicity?

“…The alterations in the activities of glutamate decarboxylase (EC 4.1.1.15; GAD), which is the sole enzyme responsible for decarboxylation of glutamate to produce GABA, and 4-aminobutyrate transaminase (EC 2.6.1.19; GABA-T), which is the major GABA degrading enzyme and also contributes to the synthesis of glutamate, seem to be inversely related in most cases. Nevertheless, in the midbrain-hippocampal region both, 4-aminobutyrate transaminase and glutamate decarboxylase, activities were stimulated by dietetic aluminium intake [98,99]. It is quite difficult to predict the impact of aluminium-induced alterations on glutamate and GABA producing and degrading enzymes in neurotransmission, since glutamate is a ubiquitous metabolite and GABA, if not used as neurotransmitter, is also easily incorporated into the citric acid cycle through the GABA shunt.…”

Preliminary Screening of a Classical Ayurvedic Formulation for Anticonvulsant Activity

“…[19] at 450 nm using commercially available ELISA kit (MBS939900; MyBioSource, Inc., San Diego, CA, USA). GABA-T was expressed as pg/mg protein.…”