Orally administrated aluminum–maltolate complex enhances oxidative stress in the organs of mice

Abstract

Recently, aluminum (Al) in drinking water has been proposed to be a risk factor for development of Alzheimer’s disease (AD). Because the physiological role of Al in humans is not yet known, we previously examined this role using an experimental animal model. Our results revealed a greater accumulation of Al in the brain, liver, kidney and spleen of mice who received long-term (90 days) administration of an Al complex, aluminum–maltolate (ALM), than in untreated controls. This observation prompted us to examine the degree of injury in the organs of mice in terms of lipid peroxidation evaluated by thiobarbituric acid reactive substances (TBARS) and NO x levels in order to determine the effects of Al accumulation. Six-week-old mice were given drinking water containing AlCl 3 or ALM for 120 days. TBARS and NO x levels were found to change depending on the organs and chemical forms of Al. In particular, TBARS and NO x levels in the brain of mice given ALM for 30, 60 and 120 days were significantly increased compared with those of the control group. In addition, nervous degeneration was detected in the brain of the ALM-treated group. These results indicate that the chemical form of Al alters the distribution and oxidative stress in the brain. In addition, we propose a more precise method of determining Al levels in biological systems using neutron activation analysis. When the biological samples are irradiated with a neutron flux, both 27Al and 31P can be counted to 28Al by the reactions, 27Al(n, γ) 28Al and 31P(n, α) 28Al, respectively. The level of Al in the organs can then be determined by subtraction of the radioactivity due to 28Al originated in 31P from the total radioactivity of the samples.