Dietary zeolite supplementation reduces oxidative damage and plaque generation in the brain of an Alzheimer's disease mouse model

Department of Biomedical Sciences and Biotechnologies, University of Brescia, 25123 Brescia, Italy. Electronic address: .
Life sciences (Impact Factor: 2.7). 04/2013; 92(17-19). DOI: 10.1016/j.lfs.2013.03.008
Source: PubMed


Oxidative stress is considered one of the main events that lead to aging and neurodegeneration. Antioxidant treatments used to counteract oxidative damage have been associated with a wide variety of side effects or at the utmost to be ineffective. The aim of the present study was to investigate the antioxidant property of a natural mineral, the tribomechanically micronized zeolite (MZ).

Main methods:
Cell death and oxidative stress were assessed in retinoic acid differentiated SH-SY5Y cells, a neuronal-like cell line, after a pro-oxidant stimulus. In vivo evaluation of antioxidant activity and amyloidogenic processing of beta amyloid have been evaluated in a transgenic model of aging related neurodegeneration, the APPswePS1dE9 transgenic mice (tg mice) after a five-month long period of water supplementation with MZ.

Key findings:
The study showed that 24h of cell pretreatment with MZ (1) protected the cells by radical oxygen species (ROS)-induced cell death and moreover (2) induced a reduction of the mitochondrial ROS production following a pro-oxidant stimulation. Looking for an antioxidant effect of MZ in vivo, we found (3) an increased activity of the endogenous antioxidant enzyme superoxide dismutase (SOD) in the hippocampus of tg mice and (4) a reduction in amyloid levels and plaque load in MZ treated tg mice compared to control tg mice.

Our results suggest MZ as a novel potential adjuvant in counteracting oxidative stress and plaque accumulation in the field of neurodegenerative diseases.

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    • "In this regard, dietary zeolite (micronized zeolite) supplementation has been shown to reduce mitochondrial ROS, increase superoxide dismutase (SOD) levels, and attenuate Aβ accumulation in the APP/PS1 mouse brain [110]. In the same way, Salvia sahendica extracts prevented reduction in the level of NRF1 and mitochondrial transcription factor A (TFAM), induced by Aβ [111]. In another study, melatonin and caffeine treatment, almost completely restored mitochondrial function in assays of respiratory rate, membrane potential, ROS production, and ATP level in the brains of the APP/PS1 [112]. "
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