scholarly journals Hormesis of Glyceollin I, an Induced Phytoalexin from Soybean, on Budding Yeast Chronological Lifespan Extension

Molecules ◽  
2014 ◽  
Vol 19 (1) ◽  
pp. 568-580 ◽  
Author(s):  
Yuancai Liu ◽  
Ziyun Wu ◽  
Shengbao Feng ◽  
Xuena Yang ◽  
Dejian Huang
2017 ◽  
Vol 4 (11) ◽  
pp. 368-375 ◽  
Author(s):  
Spike D.L. Postnikoff ◽  
Jay E. Johnson ◽  
Jessica K. Tyler

PLoS ONE ◽  
2007 ◽  
Vol 2 (8) ◽  
pp. e748 ◽  
Author(s):  
Martin Weinberger ◽  
Li Feng ◽  
Anita Paul ◽  
Daniel L. Smith ◽  
Robert D. Hontz ◽  
...  

2018 ◽  
Vol 5 (5) ◽  
pp. 233-248 ◽  
Author(s):  
Nazif Maqani ◽  
Ryan D. Fine ◽  
Mehreen Shahid ◽  
Mingguang Li ◽  
Elisa Enriquez-Hesles ◽  
...  

2018 ◽  
Vol 5 (4) ◽  
pp. 106 ◽  
Author(s):  
Zachery R. Belak ◽  
Troy Harkness ◽  
Christopher H. Eskiw

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yanjun Pan ◽  
Yanan Liu ◽  
Rui Fujii ◽  
Umer Farooq ◽  
Lihong Cheng ◽  
...  

The antiaging benzoquinone-type molecule ehretiquinone was isolated in a previous study as a leading compound from the herbal medicine Onosma bracteatum wall. This paper reports the antiaging effect and mechanism of ehretiquinone by using yeasts, mammal cells, and mice. Ehretiquinone extends not only the replicative lifespan but also the chronological lifespan of yeast and the yeast-like chronological lifespan of mammal cells. Moreover, ehretiquinone increases glutathione peroxidase, catalase, and superoxide dismutase activity and reduces reactive oxygen species and malondialdehyde (MDA) levels, contributing to the lifespan extension of the yeasts. Furthermore, ehretiquinone does not extend the replicative lifespan of Δsod1, Δsod2, Δuth1, Δskn7, Δgpx, Δcat, Δatg2, and Δatg32 mutants of yeast. Crucially, ehretiquinone induces autophagy in yeasts and mice, thereby providing significant evidence on the antiaging effects of the molecule in the mammalian level. Concomitantly, the silent information regulator 2 gene, which is known for its contributions in prolonging replicative lifespan, was confirmed to be involved in the chronological lifespan of yeasts and participates in the antiaging activity of ehretiquinone. These findings suggest that ehretiquinone shows an antiaging effect through antioxidative stress, autophagy, and histone deacetylase Sir2 regulation. Therefore, ehretiquinone is a promising molecule that could be developed as an antiaging drug or healthcare product.


2017 ◽  
Author(s):  
Sergio E. Campos ◽  
Erika Garay ◽  
J. Abraham Avelar-Rivas ◽  
Alejandro Juárez-Reyes ◽  
Alexander DeLuna

SUMMARYDietary restriction is arguably the most promising non-pharmacological intervention to extend human life and health span. Yet, only few genetic regulators mediating the cellular response to dietary restriction are known, and the question remains which other transcription factors and regulatory pathways are involved. To gain a comprehensive view of how lifespan extension under dietary restriction is elicited, we screened the chronological lifespan of most gene deletions of Saccharomyces cerevisiae under two dietary regimens, restricted and non-restricted. We identified 472 mutants with enhanced or diminished extension of lifespan by dietary restriction. Functional analysis of such dietary-restriction genes revealed novel processes underlying longevity specifically by dietary restriction. Importantly, this set of genes allowed us to generate a prioritized catalogue of transcription factors orchestrating the dietary-restriction response, which underscored the relevance of cell-cycle arrest control as a key mechanism of chronological longevity in yeast. We show that the transcription factor Ste12 is needed for full lifespan extension and cell-cycle arrest in response to nutrient limitation; linking the pheromone/invasive growth pathway with cell survivorship. Strikingly, STE12 overexpression was sufficient to extend chronological lifespan under non-restricted conditions. Our global picture of the genetic players of longevity by dietary restriction highlights intricate regulatory cross-talks in aging cells.


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