Oxido-reductive brain status after acute aluminium poisoning: The role of free radicals

Abstract

Free radicals induce oxidative processes which damage and inactivate many intracellular components and may cause cell death. This paper presents the results of experiments performed on desert mice (gerbils), adults of both sexes. After acute intraperitoneal administration of aluminium, the oxido-reductive brain state was investigated in the cerebral cortex, hippocampus and nucleus caudatus brain structures. We observed a decrease in defense capacities of the brain - decrease of superoxide dismutase and glutathione reductase activity, with a simultaneous increase in the quantity of malondialdehyde, which indicates that under the influence of aluminium the brain capacity to neutralize superoxide radicals is significantly decreased, and that the consequence is increased generation of free radicals which damage the membrane and results in the formation of malondialdehyde from membrane lipids thus breaking the functional integrity of the cell. Acute Al3+ administration caused a dose-dependent increase in the quantity of malondialdehyde in the cerebral cortex and hippocampus, while in the nucleus caudatus this effect was somewhat less pronounced. Mitochondrial superoxide dismutase was more sensitive to the administration of Al3+ than tissue superoxide dismutase.