Effects of aluminium exposure on brain glutamate and GABA systems: an experimental study in rats

• Published in: Food and chemical toxicology Vol. 39; no. 12; pp. 1285 - 1289
• Main Authors: Nayak, P, Chatterjee, A.K
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.12.2001; New York, NY Elsevier Science
• Subjects: Aluminium; Aluminum - toxicity; Animals; Biological and medical sciences; Brain; Brain - drug effects; Brain - enzymology; Brain - metabolism; Chemical and industrial products toxicology. Toxic occupational diseases; Energy Intake; GABA; GABA-T; GAD; gamma-Aminobutyric Acid - metabolism; Glutamate; Glutamate Decarboxylase - metabolism; Glutamic Acid - metabolism; Male; Medical sciences; Metals and various inorganic compounds; Rats; Rats, Wistar; SSA; Toxicology; SSA; Brain; TCA; PLP; GABA; Aluminium; GAD; GABA-T; Glutamate; MBTH; PHF; Nervous system diseases; Intraperitoneal administration; 4-Aminobutyrate transaminase; Rat; Enzyme; Toxicity; Transferases; Rodentia; Gabaergic pathway; Vertebrata; Mammalia; Transaminases; Animal; Excitatory aminoacid; Light metal; Mechanism of action; Brain (vertebrata)
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/S0278-6915(01)00077-1

It has been postulated that the neurotoxic effects of aluminium could be mediated through glutamate, an excitatory amino acid. Hence the effects of aluminium administration (at a dose of 4.2 mg/kg body weight daily as aluminium chloride, hexahydrate, intraperitoneally, for 4 weeks) on glutamate and γ-amino butyrate (GABA), an inhibitory amino acid, and related enzyme activities in different regions of the brain were studied in albino rats. The glutamate level increased significantly in the cerebrum, thalamic area, midbrain–hippocampal region and cerebellum in response to in vivo aluminium exposure. The aluminium insult also caused significant increases in glutamate α-decarboxylase activity in all the brain regions. However, on aluminium insult, the GABA content was not significantly changed except in the thalamic area, where it was elevated. On the contrary, the GABA-T activities of all the regions were reduced significantly in all regions except the midbrain–hippocampal region. However, the succinic semi-aldehyde content of all brain regions increased, often significantly. The aluminium-induced modification of the enzyme activities may be either due to the direct impact of aluminium or due to aluminium-induced changes in the cellular environment. The aluminium-induced differential regional accumulation of glutamate or other alterations in enzymes of the glutamate–GABA system may be one of the causes of aluminium-induced neurotoxicity.