scholarly journals Glutathione levels influence chronological life span of Saccharomyces cerevisiae in a glucose-dependent manner

2017 ◽  
Author(s):  
Mayra Fabiola Tello-Padilla ◽  
Alejandra Yudid Perez-Gonzalez ◽  
Melina Canizal-García ◽  
Juan Carlos González-Hernández ◽  
Christian Cortes-Rojo ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Dietary Restriction ◽  
Aging Process ◽  
Chemical Species ◽  
Ros Generation ◽  
Dependent Manner ◽  
Transport Chain ◽  
Chronological Life Span ◽  
Glucose Restriction

AbstractDiet plays a key role in determining the longevity of the organisms since it has been demonstrated that glucose restriction increases lifespan whereas a high-glucose diet decreases it. However, the molecular basis of how diet leads to the aging process is currently unknown. We propose that the quantity of glucose that fuels respiration influences ROS generation and glutathione levels, and both chemical species impact in the aging process. Herein, we provide evidence that mutation of the gene GSH1 diminishes glutathione levels. Moreover, glutathione levels were higher with 0.5% than in 10% glucose in the gsh1Δ and WT strains. Interestingly, the chronological life span (CLS) was lowered in the gsh1Δ strain cultured with 10% glucose but not under dietary restriction. The gsh1Δ strain also showed an inhibition of the mitochondrial respiration in 0.5 and 10% of glucose but only increased the H2O2 levels under dietary restriction. These results correlate well with the GSH/GSSG ratio, which showed a decrease in gsh1Δ strain cultured with 0.5% glucose. Altogether these data indicate that glutathione has a major role in the function of electron transport chain (ETC) and is essential to maintain life span of Saccharomyces cerevisiae in 10% glucose.

scholarly journals Resveratrol induces mitochondrial dysfunction and decreases chronological life span of Saccharomyces cerevisiae in a glucose-dependent manner

2017 ◽  
Vol 49 (3) ◽  
pp. 241-251 ◽  
Author(s):  
Minerva Ramos-Gomez ◽  
Ivanna Karina Olivares-Marin ◽  
Melina Canizal-García ◽  
Juan Carlos González-Hernández ◽  
Gerardo M. Nava ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Mitochondrial Dysfunction ◽  
Dependent Manner ◽  
Chronological Life Span

scholarly journals Resveratrol induces mitochondrial dysfunction and decreases chronological life span of Saccharomyces cerevisiae in a glucose-dependent manner

2017 ◽  
Author(s):  
Minerva Ramos-Gomez ◽  
Ivanna Karina Olivares-Marin ◽  
Melina Canizal-García ◽  
Juan Carlos González-Hernández ◽  
Gerardo M. Nava ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Oxygen Consumption ◽  
Life Span ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane ◽  
Exponential Phase ◽  
Dependent Manner ◽  
Yeast Cultures ◽  
Chronological Life Span ◽  
High Level

AbstractA broad range of health benefits have been attributed to resveratrol (RSV) supplementation in mammalian systems, including the increases in longevity. Nonetheless, despite the growing number of studies performed with RSV, the molecular mechanism by which it acts still remains unknown. Recently, it has been proposed that inhibition of the oxidative phosphorylation activity is the principal mechanism of RSV action. This mechanism suggests that RSV might induce mitochondrial dysfunction resulting in oxidative damage to cells with a concomitant decrease of cell viability and cellular life span. To prove this hypothesis, the chronological life span (CLS) of Saccharomyces cerevisiae was studied as it is accepted as an important model of oxidative damage and aging. In addition, oxygen consumption, mitochondrial membrane potential, and hydrogen peroxide (H2O2) release were measured in order to determine the extent of mitochondrial dysfunction. The results demonstrated that the supplementation of S. cerevisiae cultures with 100 μM RSV decreased CLS in a glucose-dependent manner. At high-level glucose, RSV supplementation increased oxygen consumption during the exponential phase yeast cultures, but inhibited it in chronologically aged yeast cultures. However, at low-level glucose, oxygen consumption was inhibited in yeast cultures in the exponential phase as well as in chronologically aged cultures. Furthermore, RSV supplementation promoted the polarization of the mitochondrial membrane in both cultures. Finally, RSV decreased the release of H2O2 with high-level glucose and increased it at low-level glucose. Altogether, this data supports the hypothesis that RSV supplementation decreases CLS as a result of mitochondrial dysfunction and this phenotype occurs in a glucose-dependent manner.

Magnolol protects Saccharomyces cerevisiae antioxidant-deficient mutants from oxidative stress and extends yeast chronological life span

2019 ◽  
Vol 366 (8) ◽  
Author(s):  
Subasri Subramaniyan ◽  
Phaniendra Alugoju ◽  
Sudharshan SJ ◽  
Bhavana Veerabhadrappa ◽  
Madhu Dyavaiah
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Chronological Life Span

scholarly journals PCK1 Deficiency Shortens the Replicative Lifespan of Saccharomyces cerevisiae through Upregulation of PFK1

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yuan Yuan ◽  
Jia-ying Lin ◽  
Hong-jing Cui ◽  
Wei Zhao ◽  
Hui-ling Zheng ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Glucose Metabolism ◽  
Aging Process ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Critical Role ◽  
Ros Generation ◽  
High Throughput Analysis ◽  
Replicative Lifespan ◽  
Regulatory Pathways ◽  
Glucose Levels

The cytosolic isozyme of phosphoenolpyruvate carboxykinase (PCK1) was the first rate-limiting enzyme in the gluconeogenesis pathway, which exerted a critical role in maintaining the blood glucose levels. PCK1 has been established to be involved in various physiological and pathological processes, including glucose metabolism, lipid metabolism, diabetes, and tumorigenesis. Nonetheless, the association of PCK1 with aging process and the detailed underlying mechanisms of PCK1 on aging are still far to be elucidated. Hence, we herein constructed the PCK1-deficient (pck1Δ) and PCK1 overexpression (PCK1 OE) Saccharomyces cerevisiae. The results unveiled that PCK1 deficiency significantly shortened the replicative lifespan (RLS) in the S. cerevisiae, while overexpression of PCK1 prolonged the RLS. Additionally, we noted that the ROS level was significantly enhanced in PCK1-deficient strain and decreased in PCK1 OE strain. Then, a high throughput analysis by deep sequencing was performed in the pck1Δ and wild-type strains, in an attempt to shed light on the effect of PCK1 on the lifespan of aging process. The data showed that the most downregulated mRNAs were enriched in the regulatory pathways of glucose metabolism. Fascinatingly, among the differentially expressed mRNAs, PFK1 was one of the most upregulated genes, which was involved in the glycolysis process and ROS generation. Thus, we further constructed the pfk1Δpck1Δ strain by deletion of PFK1 in the PCK1-deficient strain. The results unraveled that pfk1Δpck1Δ strain significantly suppressed the ROS level and restored the RLS of pck1Δ strain. Taken together, our data suggested that PCK1 deficiency enhanced the ROS level and shortened the RLS of S. cerevisiae via PFK1.

scholarly journals The chronological life span of Saccharomyces cerevisiae

Aging Cell ◽  
2003 ◽  
Vol 2 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Paola Fabrizio ◽  
Valter D. Longo
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Chronological Life Span

scholarly journals Identification of Tropical Plant Extracts That Extend Yeast Chronological Life Span

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2718
Author(s):  
Mandy Mun Yee Kwong ◽  
Jee Whu Lee ◽  
Mohammed Razip Samian ◽  
Habibah A. Wahab ◽  
Nobumoto Watanabe ◽  
...  
Keyword(s):  
Life Span ◽  
Plant Extracts ◽  
Stress Resistance ◽  
Manihot Esculenta ◽  
Dependent Manner ◽  
Leaf Extracts ◽  
Cellular Processes ◽  
Tropical Plant ◽  
Chronological Life Span ◽  
Dose Dependent

Certain plant extracts (PEs) contain bioactive compounds that have antioxidant and lifespan-extending activities on organisms. These PEs play different roles in cellular processes, such as enhancing stress resistance and modulating longevity-defined signaling pathways that contribute to longevity. Here, we report the discovery of PEs that extended chronological life span (CLS) in budding yeast from a screen of 222 PEs. We identified two PEs, the leaf extracts of Manihot esculenta and Wodyetia bifurcata that extended CLS in a dose-dependent manner. The CLS-extending PEs also conferred oxidative stress tolerance, suggesting that these PEs might extend yeast CLS through the upregulation of stress response pathways.

scholarly journals Mitochondrial small heat shock protein mediates seed germination via thermal sensing

2019 ◽  
Vol 116 (10) ◽  
pp. 4716-4721 ◽  
Author(s):  
Wei Ma ◽  
Xueying Guan ◽  
Jie Li ◽  
Ronghui Pan ◽  
Luyao Wang ◽  
...  
Keyword(s):  
Heat Shock ◽  
Seed Germination ◽  
Heat Shock Protein ◽  
Critical Factor ◽  
Small Heat Shock Protein ◽  
Ros Generation ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Transport Chain ◽  
Thermal Sensing

Seed germination is an energy demanding process that requires functional mitochondria upon imbibition. However, how mitochondria fine tune seed germination, especially in response to the dynamics of environmental temperature, remains largely unknown at the molecular level. Here, we report a mitochondrial matrix-localized heat shock protein GhHSP24.7, that regulates seed germination in a temperature-dependent manner. Suppression ofGhHSP24.7renders the seed insensitive to temperature changes and delays germination. We show that GhHSP24.7 competes with GhCCMH to bind to the maturation subunit protein GhCcmFcto form cytochrome C/C1(CytC/C1) in the mitochondrial electron transport chain. GhHSP24.7 modulates CytC/C1production to induce reactive oxygen species (ROS) generation, which consequently accelerates endosperm rupture and promotes seed germination. Overexpression ofGhHSP24.7’s homologous genes can accelerate seed germination inArabidopsisand tomato, indicating its conserved function across plant species. Therefore,HSP24.7is a critical factor that positively controls seed germination via temperature-dependent ROS generation.

scholarly journals Farnesol-Induced Generation of Reactive Oxygen Species via Indirect Inhibition of the Mitochondrial Electron Transport Chain in the Yeast Saccharomyces cerevisiae

1998 ◽  
Vol 180 (17) ◽  
pp. 4460-4465 ◽  
Author(s):  
Kiyotaka Machida ◽  
Toshio Tanaka ◽  
Ken-ichi Fujita ◽  
Makoto Taniguchi
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Electron Transport ◽  
Growth Inhibition ◽  
Electron Transport Chain ◽  
Complex Iii ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain

ABSTRACT The mechanism of farnesol (FOH)-induced growth inhibition ofSaccharomyces cerevisiae was studied in terms of its promotive effect on generation of reactive oxygen species (ROS). The level of ROS generation in FOH-treated cells increased five- to eightfold upon the initial 30-min incubation, while cells treated with other isoprenoid compounds, like geraniol, geranylgeraniol, and squalene, showed no ROS-generating response. The dependence of FOH-induced growth inhibition on such an oxidative stress was confirmed by the protection against such growth inhibition in the presence of an antioxidant such as α-tocopherol, probucol, orN-acetylcysteine. FOH could accelerate ROS generation only in cells of the wild-type grande strain, not in those of the respiration-deficient petite mutant ([rho 0]), which illustrates the role of the mitochondrial electron transport chain as its origin. Among the respiratory chain inhibitors, ROS generation could be effectively eliminated with myxothiazol, which inhibits oxidation of ubiquinol to the ubisemiquinone radical by the Rieske iron-sulfur center of complex III, but not with antimycin A, an inhibitor of electron transport that is functional in further oxidation of the ubisemiquinone radical to ubiquinone in the Q cycle of complex III. Cellular oxygen consumption was inhibited immediately upon extracellular addition of FOH, whereas FOH and its possible metabolites failed to directly inhibit any oxidase activities detected with the isolated mitochondrial preparation. A protein kinase C (PKC)-dependent mechanism was suggested to exist in the inhibition of mitochondrial electron transport since FOH-induced ROS generation could be effectively eliminated with a membrane-permeable diacylglycerol analog which can activate PKC. The present study supports the idea that FOH inhibits the ability of the electron transport chain to accelerate ROS production via interference with a phosphatidylinositol type of signal.

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