Aluminum chloride induced oxidative damage on cells derived from hippocampus and cortex of ICR mice

Abstract

Aluminum (Al) is among the most abundant elements on earth, it has been associated with the etiology of Alzheimer's disease. In the present study, AlCl(3) was administered with the dose of 10, 50 or 300 mg/kg b.wt/day through diet for 100 days. On day 101, overnight-fasted animals were sacrificed, the whole brains were removed and the cells from hippocampus or cortex were separated for the measurements: malondialdehyde (MDA), superoxide dismutase (SOD), nuclear DNA (nDNA) and mitochondrial DNA (mtDNA) damage. AlCl(3) exposure resulted in increased MDA levels accompanied by decreased activities of SOD in the cells. Comet assay demonstrated that aluminum induces nDNA damage in a dose-dependent manner, dramatically increased formation of 8-hydroxy 2-deoxyguanosine (8-OHdG) in the mtDNA isolated from the cells was also measured. The alterations seem more serious than the results displayed by the studies performed with lower doses of aluminum. However, a detailed biochemical mechanism by which aluminum accelerates mtDNA damage has not yet been identified, but the decrease in superoxide dismutase (SOD) activity and increase in MDA level in aluminum-treated mice may suggest the involvement of oxidative stress.