Dihydrolipoyl dehydrogenase as a source of reactive oxygen species inhibited by caloric restriction and involved in Saccharomyces cerevisiae aging

2006 ◽  
Vol 21 (1) ◽  
pp. 274-283 ◽  
Author(s):  
Erich B. Tahara ◽  
Mario H. Barros ◽  
Graciele A. Oliveira ◽  
Luis E. S. Netto ◽  
Alicia J. Kowaltowski
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Caloric Restriction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dihydrolipoyl Dehydrogenase

Induction of reactive oxygen species by diphenyl diselenide is preceded by changes in cell morphology and permeability in Saccharomyces cerevisiae

2017 ◽  
Vol 51 (7-8) ◽  
pp. 657-668 ◽  
Author(s):  
Leticia Selinger Galant ◽  
Marcos Martins Braga ◽  
Diego de Souza ◽  
Andreza Fabro de Bem ◽  
Luca Sancineto ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Cell Morphology ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diphenyl Diselenide

scholarly journals Reactive oxygen species (ROS) mediated enhanced anti-candidal activity of ZnS–ZnO nanocomposites with low inhibitory concentrations

RSC Advances ◽  
2015 ◽  
Vol 5 (94) ◽  
pp. 76718-76728 ◽  
Author(s):  
P. Suyana ◽  
S. Nishanth Kumar ◽  
Nimisha Madhavan ◽  
B. S. Dileep Kumar ◽  
Balagopal N. Nair ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Candida Albicans ◽  
Antifungal Activity ◽  
Candida Tropicalis ◽  
Yeast Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Precipitation Technique

Enhanced antifungal activity against the yeast species Candida albicans, Candida tropicalis and Saccharomyces cerevisiae was displayed by ZnS–ZnO nanocomposites prepared by a simple precipitation technique.

scholarly journals Lipid droplets alleviate cadmium induced cytotoxicity in Saccharomyces cerevisiae

2017 ◽  
Vol 6 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Selvaraj Rajakumar ◽  
Vasanthi Nachiappan
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Lipid Droplets ◽  
Reactive Oxygen ◽  
Oxygen Species

Cadmium (Cd) induces oxidative stress that generates reactive oxygen species (ROS) and increased lipid accumulation.

The novel equisetin-like compound, TA-289, causes aberrant mitochondrial morphology which is independent of the production of reactive oxygen species in Saccharomyces cerevisiae

2013 ◽  
Vol 9 (8) ◽  
pp. 2125 ◽  
Author(s):  
Natelle C. H. Quek ◽  
James H. Matthews ◽  
Stephen J. Bloor ◽  
Darryl A. Jones ◽  
Peter W. Bircham ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Morphology ◽  
Oxygen Species ◽  
The Novel

scholarly journals A Chemogenomic Screen in Saccharomyces cerevisiae Uncovers a Primary Role for the Mitochondria in Farnesol Toxicity and Its Regulation by the Pkc1 Pathway

2006 ◽  
Vol 282 (7) ◽  
pp. 4868-4874 ◽  
Author(s):  
Gregory D. Fairn ◽  
Kendra MacDonald ◽  
Christopher R. McMaster
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Electron Transport ◽  
Signaling Pathway ◽  
Electron Transport Chain ◽  
Reactive Oxygen ◽  
Complex Iii ◽  
Oxygen Species ◽  
Transport Chain

The isoprenoid farnesol has been shown to preferentially induce apoptosis in cancerous cells; however, the mode of action of farnesol-induced death is not established. We used chemogenomic profiling using Saccharomyces cerevisiae to probe the core cellular processes targeted by farnesol. This screen revealed 48 genes whose inactivation increased sensitivity to farnesol. The gene set indicated a role for the generation of oxygen radicals by the Rieske iron-sulfur component of complex III of the electron transport chain as a major mediator of farnesol-induced cell death. Consistent with this, loss of mitochondrial DNA, which abolishes electron transport, resulted in robust resistance to farnesol. A genomic interaction map predicted interconnectedness between the Pkc1 signaling pathway and farnesol sensitivity via regulation of the generation of reactive oxygen species. Consistent with this prediction (i) Pkc1, Bck1, and Mkk1 relocalized to the mitochondria upon farnesol addition, (ii) inactivation of the only non-essential and non-redundant member of the Pkc1 signaling pathway, BCK1, resulted in farnesol sensitivity, and (iii) expression of activated alleles of PKC1, BCK1, and MKK1 increased resistance to farnesol and hydrogen peroxide. Sensitivity to farnesol was not affected by the presence of the osmostabilizer sorbitol nor did farnesol affect phosphorylation of the ultimate Pkc1-responsive kinase responsible for controlling the cell wall integrity pathway, Slt2. The data indicate that the generation of reactive oxygen species by the electron transport chain is a primary mechanism by which farnesol kills cells. The Pkc1 signaling pathway regulates farnesol-mediated cell death through management of the generation of reactive oxygen species.

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