Abstract

Even though aluminium is not considered to be a heavy metal like lead, silver, arsenic and cadmium, it can be toxic when taken in excessive amounts and even in small amounts if deposited in the brain. Glutathione, a major antioxidant in the cells, so its depletion weakens the tissue resistance to oxidant. Glutathione is the sulfhydryl (-SH) antioxidant, antitoxin and enzyme cofactor which plays an important role in aluminum detoxification. The present study was designed to investigate the extent of changes in glutathione level by inorganic and organic alumni metal. Biocordination of aluminum acetylacetonate and aluminum sulphate with glutathione in T-cells and b-cells of lymphocytes have been described using Ellman’s method. The decline of glutathione level is due to increased aluminum concentration and time of incubation. The decline of glutathione level was consistent with increasing pH, while at physiological temperature, the drop was more significant. Our study indicates that changes in glutathione level produced by aluminium could be due to conjugate (Al-(SG)₃) formation. This change in glutathione level endowed with information regarding mechanism of toxicity of aluminium inorganic and organic complexes. This study is important for the design of rational antidote for the prevention of aluminium toxicity.

Key words: Glutathione (GSH), aluminium sulphate Al₂(SO₄)₃, aluminium acetylacetonate (Al(acac)₃) , T-cells, B-cells.