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Low molecular proanthocyanidin dietary biofactor Oligonol: Its modulation of oxidative stress, bioefficacy, neuroprotection, food application and chemoprevention potentials

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Authors

Aruoma, Okezie I.; Sun, Buxiang; Fujii, Hajime; Neergheen, Vidushi S.; Bahorun, Theeshan; Kang, Kyung-Sun; Sung, Mi-Kyung

Issue Date
2006
Publisher
Wiley-Blackwell
International Union of Biochemistry and Molecular Biology
Citation
BioFactors 27 (2006), 245-265
Keywords
Oligonolneurodegenerative diseasesanti-aging prophylactic agentmetabolic disordersfunctional foodsAge-dependent disordersflavonoidsredox biochemistryinflammation and cell signalingchemopreventionneuroprotection
Abstract
Interdisciplinary research endeavors are directed at understanding the molecular mechanisms of neurodegenerative and chronic diseases that affect human lifestyle. Hence the potential for developing medicinal herb-derived and food plant-derived prophylactic agents directed at neurological, metabolic, cardiovascular and psychiatric disorders abounds. Oligonol is a novel technology product emanating from the oligomerization of polyphenols, typically proanthocyanidin from a variety of fruits (grapes, apples, persimmons etc.) that has optimized bioavailability. It is an optimized phenolic product containing catechin-type monomers and oligomeric proanthocyanidins, the easily absorbed forms. Typically the constituents of Oligonol are 15-20% monomers, 8-12% dimers and 5-10% trimers. Supplementation of mice with Oligonol prior to the administration of ferric-nitrilotriacetic complex (a Fenton chemistry model) significantly reduced the extent of lipid peroxidation in the kidney, brain and liver. Oligonol triggers apoptosis in the MCF-7 and MDA-MB-231 breast cancer cells through modulation of the pro-apoptotic Bcl-2 family of proteins and the MEK/ERK signaling pathway, an observation suggesting its important chemopreventive effects. The senescence-accelerated strain of mice (SAM) are models of senescence acceleration and geriatric disorders which exhibit learning and memory deficits and enhanced production or defective control of oxidative stress leading.
ISSN
0951-6433 (print)
1872-8081 (online)
Language
English
URI
https://hdl.handle.net/10371/6508
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