Soy isoflavone glycitein protects against beta amyloid-induced toxicity and oxidative stress in transgenic Caenorhabditis elegans
1 Department of Biological Sciences, University of Southern Mississippi, Hattiesburg, MS 39406, USA
2 Department of Human Sciences, Alcorn State University, Alcorn, MS 39096, USA
3 National Center for Natural Products Research, School of Pharmacy, Oxford, MS 38655, USA
4 Institute for Behavioral Genetic, University of Colorado, Boulder CO 80309, USA
5 Laboratory of Visual Information Processing, Center of Brain & Cognitive Science, Institute of Biophysics, Academia Sinica, Beijing 100101, P.R. China
6 Department of Pharmaceutical Science, School of Pharmacy, University of Maryland, Baltimore, MD 21201-1180, USA
BMC Neuroscience 2005, 6:54 doi:10.1186/1471-2202-6-54Published: 25 August 2005
Epidemiological studies have associated estrogen replacement therapy with a lower risk of developing Alzheimer's disease, but a higher risk of developing breast cancer and certain cardiovascular disorders. The neuroprotective effect of estrogen prompted us to determine potential therapeutic impact of soy-derived estrogenic compounds. Transgenic C. elegans, that express human beta amyloid (Aβ), were fed with soy derived isoflavones genistein, daidzein and glycitein (100 μg/ml) and then examined for Aβ-induced paralysis and the levels of reactive oxygen species.
Among the three compounds tested, only glycitein alleviated Aβ expression-induced paralysis in the transgenic C. elegans. This activity of glycitein correlated with a reduced level of hydrogen peroxide in the transgenic C. elegans. In vitro scavenging effects of glycitein on three types of reactive oxygen species confirmed its antioxidant properties. Furthermore, the transgenic C. elegans fed with glycitein exhibited reduced formation of β amyloid.
These findings suggest that a specific soy isoflavone glycitein may suppress Aβ toxicity through combined antioxidative activity and inhibition of Aβ deposition, thus may have therapeutic potential for prevention of Aβ associated neurodegenerative disorders.