scholarly journals The Mechanisms of Thiosulfate Toxicity against Saccharomyces cerevisiae

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 646
Author(s):  
Zhigang Chen ◽  
Yongzhen Xia ◽  
Huaiwei Liu ◽  
Honglei Liu ◽  
Luying Xun
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Mitochondrial Membrane ◽  
Deletion Mutant ◽  
Elemental Sulfur ◽  
Yeast Mitochondria ◽  
Wild Type ◽  
Sulfurous Acid ◽  
Transport Chain

Elemental sulfur and sulfite have been used to inhibit the growth of yeasts, but thiosulfate has not been reported to be toxic to yeasts. We observed that thiosulfate was more inhibitory than sulfite to Saccharomyces cerevisiae growing in a common yeast medium. At pH < 4, thiosulfate was a source of elemental sulfur and sulfurous acid, and both were highly toxic to the yeast. At pH 6, thiosulfate directly inhibited the electron transport chain in yeast mitochondria, leading to reductions in oxygen consumption, mitochondrial membrane potential and cellular ATP. Although thiosulfate was converted to sulfite and H2S by the mitochondrial rhodanese Rdl1, its toxicity was not due to H2S as the rdl1-deletion mutant that produced significantly less H2S was more sensitive to thiosulfate than the wild type. Evidence suggests that thiosulfate inhibits cytochrome c oxidase of the electron transport chain in yeast mitochondria. Thus, thiosulfate is a potential agent against yeasts.

scholarly journals Palmitic Acid, but Not Lauric Acid, Induces Metabolic Inflammation, Mitochondrial Fragmentation, and a Drop in Mitochondrial Membrane Potential in Human Primary Myotubes

2021 ◽  
Vol 8 ◽  
Author(s):  
Domenico Sergi ◽  
Natalie Luscombe-Marsh ◽  
Nenad Naumovski ◽  
Mahinda Abeywardena ◽  
Nathan O'Callaghan
Keyword(s):  
Insulin Resistance ◽  
Membrane Potential ◽  
Electron Transport ◽  
Mitochondrial Membrane Potential ◽  
Electron Transport Chain ◽  
Mitochondrial Membrane ◽  
Chain Complex ◽  
Mitochondrial Fragmentation ◽  
Metabolic Inflammation ◽  
Transport Chain

The chain length of saturated fatty acids may dictate their impact on inflammation and mitochondrial dysfunction, two pivotal players in the pathogenesis of insulin resistance. However, these paradigms have only been investigated in animal models and cell lines so far. Thus, the aim of this study was to compare the effect of palmitic (PA) (16:0) and lauric (LA) (12:0) acid on human primary myotubes mitochondrial health and metabolic inflammation. Human primary myotubes were challenged with either PA or LA (500 μM). After 24 h, the expression of interleukin 6 (IL-6) was assessed by quantitative polymerase chain reaction (PCR), whereas Western blot was used to quantify the abundance of the inhibitor of nuclear factor κB (IκBα), electron transport chain complex proteins and mitofusin-2 (MFN-2). Mitochondrial membrane potential and dynamics were evaluated using tetraethylbenzimidazolylcarbocyanine iodide (JC-1) and immunocytochemistry, respectively. PA, contrarily to LA, triggered an inflammatory response marked by the upregulation of IL-6 mRNA (11-fold; P &lt; 0.01) and a decrease in IκBα (32%; P &lt; 0.05). Furthermore, whereas PA and LA did not differently modulate the levels of mitochondrial electron transport chain complex proteins, PA induced mitochondrial fragmentation (37%; P &lt; 0.001), decreased MFN-2 (38%; P &lt; 0.05), and caused a drop in mitochondrial membrane potential (11%; P &lt; 0.01) compared to control, with this effect being absent in LA-treated cells. Thus, LA, as opposed to PA, did not trigger pathogenetic mechanisms proposed to be linked with insulin resistance and therefore represents a healthier saturated fatty acid choice to potentially preserve skeletal muscle metabolic health.

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.

scholarly journals CHLOROPLAST STRUCTURE AND FUNCTION IN ac-20, A MUTANT STRAIN OF CHLAMYDOMONAS REINHARDI

1970 ◽  
Vol 44 (3) ◽  
pp. 540-546 ◽  
Author(s):  
R. P. Levine ◽  
A. Paszewski
Keyword(s):  
Electron Transport ◽  
Mutant Strain ◽  
Electron Transport Chain ◽  
Co2 Fixation ◽  
Photosynthetic Electron Transport ◽  
Structure And Function ◽  
Wild Type ◽  
Carboxylase Activity ◽  
Transport Chain ◽  
And Function

Photosynthetic electron transport is markedly affected in mixotrophic cells of ac-20 because they lack the capacity to form the wild-type level of cytochrome 559, as well as Q, the quencher of fluorescence of photochemical system II. The other components of the electron-transport chain, as well as reactions dependent upon photochemical system I, are unaffected in the mutant strain. These observations are discussed in terms of the previously reported effects of the ac-20 mutation on CO2 fixation and ribulose-1,5-diphosphate carboxylase activity.

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.

Iba57p participates in maturation of a [2Fe–2S]-cluster Rieske protein and in formation of supercomplexes III/IV of Saccharomyces cerevisiae electron transport chain

Mitochondrion ◽  
2019 ◽  
Vol 44 ◽  
pp. 75-84 ◽  
Author(s):  
Luis A. Sánchez ◽  
Mauricio Gómez-Gallardo ◽  
Alma L. Díaz-Pérez ◽  
Christian Cortés-Rojo ◽  
Jesús Campos-García
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Rieske Protein ◽  
Transport Chain
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