Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.

Hormesis occurs when a low level stress elicits adaptive beneficial responses that protect against subsequent exposure to severe stress. Recent findings suggest that mild oxidative and thermal stress can extend lifespan by hormetic mechanisms. Here we show that the botanical pesticide plumbagin, whi...

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Autores principales:	Piper R Hunt, Tae Gen Son, Mark A Wilson, Quian-Sheng Yu, William H Wood, Yongqing Zhang, Kevin G Becker, Nigel H Greig, Mark P Mattson, Simonetta Camandola, Catherine A Wolkow
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/310115c5f568487eb992a24b39623b79
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spelling	oai:doaj.org-article:310115c5f568487eb992a24b39623b792021-11-18T06:50:21ZExtension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.1932-620310.1371/journal.pone.0021922https://doaj.org/article/310115c5f568487eb992a24b39623b792011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21765926/?tool=EBIhttps://doaj.org/toc/1932-6203Hormesis occurs when a low level stress elicits adaptive beneficial responses that protect against subsequent exposure to severe stress. Recent findings suggest that mild oxidative and thermal stress can extend lifespan by hormetic mechanisms. Here we show that the botanical pesticide plumbagin, while toxic to C. elegans nematodes at high doses, extends lifespan at low doses. Because plumbagin is a naphthoquinone that can generate free radicals in vivo, we investigated whether it extends lifespan by activating an adaptive cellular stress response pathway. The C. elegans cap'n'collar (CNC) transcription factor, SKN-1, mediates protective responses to oxidative stress. Genetic analysis showed that skn-1 activity is required for lifespan extension by low-dose plumbagin in C. elegans. Further screening of a series of plumbagin analogs identified three additional naphthoquinones that could induce SKN-1 targets in C. elegans. Naphthazarin showed skn-1dependent lifespan extension, over an extended dose range compared to plumbagin, while the other naphthoquinones, oxoline and menadione, had differing effects on C. elegans survival and failed to activate ARE reporter expression in cultured mammalian cells. Our findings reveal the potential for low doses of naturally occurring naphthoquinones to extend lifespan by engaging a specific adaptive cellular stress response pathway.Piper R HuntTae Gen SonMark A WilsonQuian-Sheng YuWilliam H WoodYongqing ZhangKevin G BeckerNigel H GreigMark P MattsonSimonetta CamandolaCatherine A WolkowPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 7, p e21922 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Piper R Hunt Tae Gen Son Mark A Wilson Quian-Sheng Yu William H Wood Yongqing Zhang Kevin G Becker Nigel H Greig Mark P Mattson Simonetta Camandola Catherine A Wolkow Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
description	Hormesis occurs when a low level stress elicits adaptive beneficial responses that protect against subsequent exposure to severe stress. Recent findings suggest that mild oxidative and thermal stress can extend lifespan by hormetic mechanisms. Here we show that the botanical pesticide plumbagin, while toxic to C. elegans nematodes at high doses, extends lifespan at low doses. Because plumbagin is a naphthoquinone that can generate free radicals in vivo, we investigated whether it extends lifespan by activating an adaptive cellular stress response pathway. The C. elegans cap'n'collar (CNC) transcription factor, SKN-1, mediates protective responses to oxidative stress. Genetic analysis showed that skn-1 activity is required for lifespan extension by low-dose plumbagin in C. elegans. Further screening of a series of plumbagin analogs identified three additional naphthoquinones that could induce SKN-1 targets in C. elegans. Naphthazarin showed skn-1dependent lifespan extension, over an extended dose range compared to plumbagin, while the other naphthoquinones, oxoline and menadione, had differing effects on C. elegans survival and failed to activate ARE reporter expression in cultured mammalian cells. Our findings reveal the potential for low doses of naturally occurring naphthoquinones to extend lifespan by engaging a specific adaptive cellular stress response pathway.
format	article
author	Piper R Hunt Tae Gen Son Mark A Wilson Quian-Sheng Yu William H Wood Yongqing Zhang Kevin G Becker Nigel H Greig Mark P Mattson Simonetta Camandola Catherine A Wolkow
author_facet	Piper R Hunt Tae Gen Son Mark A Wilson Quian-Sheng Yu William H Wood Yongqing Zhang Kevin G Becker Nigel H Greig Mark P Mattson Simonetta Camandola Catherine A Wolkow
author_sort	Piper R Hunt
title	Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
title_short	Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
title_full	Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
title_fullStr	Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
title_full_unstemmed	Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.
title_sort	extension of lifespan in c. elegans by naphthoquinones that act through stress hormesis mechanisms.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/310115c5f568487eb992a24b39623b79
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Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms.

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