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Article Publish Status: FREE
Abstract Title:

Vitamin Bdeficiency results in severe oxidative stress, leading to memory retention impairment in Caenorhabditis elegans.

Abstract Source:

Redox Biol. 2017 04 ;11:21-29. Epub 2016 Nov 3. PMID: 27840283

Abstract Author(s):

Tomohiro Bito, Taihei Misaki, Yukinori Yabuta, Takahiro Ishikawa, Tsuyoshi Kawano, Fumio Watanabe

Article Affiliation:

Tomohiro Bito

Abstract:

Oxidative stress is implicated in various human diseases and conditions, such as a neurodegeneration, which is the major symptom of vitamin Bdeficiency, although the underlying disease mechanisms associated with vitamin Bdeficiency are poorly understood. Vitamin Bdeficiency was found to significantly increase cellular HOand NO content in Caenorhabditis elegans and significantly decrease low molecular antioxidant [reduced glutathione (GSH) and L-ascorbic acid] levels and antioxidant enzyme (superoxide dismutase and catalase) activities, indicating that vitamin Bdeficiency induces severe oxidative stress leading to oxidative damage of various cellular components in worms. An NaCl chemotaxis associative learning assay indicated that vitamin Bdeficiency did not affect learning ability but impaired memory retention ability, which decreased to approximately 58% of the control value. When worms were treated with 1mmol/L GSH, L-ascorbic acid, or vitamin E for three generations during vitamin Bdeficiency, cellular malondialdehyde content as an index of oxidative stress decreased to the control level, but the impairment of memory retention ability was not completely reversed (up to approximately 50%). These results suggest that memory retention impairment formed during vitamin Bdeficiency is partially attributable to oxidative stress.

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