Regular consumption of a silicic acid-rich water prevents aluminium-induced alterations of nitrergic neurons in mouse brain: histochemical and immunohistochemical studies

• Published in: Histology and histopathology Vol. 27; no. 8; p. 1055
• Main Authors: Foglio, E, Buffoli, B, Exley, C, Rezzani, R, Rodella, L F
• Format: Journal Article
• Language: English
• Published: Spain 01-08-2012
• Subjects: Alum Compounds - analysis; Alum Compounds - toxicity; Animals; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Drinking; Drinking Water - chemistry; Drug Antagonism; Male; Mice; Mice, Inbred C57BL; Mineral Waters - analysis; NADPH Dehydrogenase - metabolism; Neuroprotective Agents - pharmacology; Nitrergic Neurons - drug effects; Nitrergic Neurons - metabolism; Nitrergic Neurons - pathology; Nitric Oxide Synthase Type I - metabolism; Silicic Acid - pharmacology; Toxicity Tests, Chronic; Water Pollutants, Chemical - analysis; Water Pollutants, Chemical - toxicity
• ISSN: 1699-5848
• DOI: 10.14670/HH-27.1055

Silicon is not generally considered an essential nutrient for mammals and, to date, whether it has a biological role or beneficial effects in humans is not known. The results of a number of studies suggest that dietary silicon supplementation might have a protective effect both for limiting aluminium absorption across the gut and for the removal of systemic aluminium via the urine, hence, preventing potential accumulation of aluminium in the brain. Since our previous studies demonstrated that aluminium exposure reduces the number of nitrergic neurons, the aim of the present study was to compare the distribution and the morphology of NO-containing neurons in brain cortex of mice exposed to aluminium sulphate dissolved in silicic acid-rich or poor drinking water to assess the potential protective role of silicon against aluminium toxicity in the brain. NADPH-d histochemistry and nNOS immunohistochemistry showed that high concentrations of silicon in drinking water were able to minimize the impairment of the function of nitrergic neurons induced by aluminium administration. We found that silicon protected against aluminium-induced damage to the nitrergic system: in particular, we demonstrated that silicon maintains the number of nitrergic neurons and their expression of nitrergic enzymes at physiological levels, even after a 12 and 15 month exposure to aluminium.