Mitochondrial and nuclear genomic integrity after oxidative damage in Saccharomyces cerevisiae

Yazgan, Oya; Krebs, Jocelyn E.

doi:10.2741/3974

Cited by 15 publications

(16 citation statements)

References 108 publications

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“…The leakage of electrons from the mitochondrial respiratory chain is pointed out as the main source of endogenous ROS in S. cerevisiae. However, S. cerevisiae is known to tolerate the loss of mtDNA (Yazgan and Krebs 2012), which makes this organism a useful model to evaluate how the mitochondrial respiratory chain is involved in Pb-induced oxidative stress. Thus, to evaluate whether mitochondrial function was the source of Pb-induced oxidative stress and, consequently, was associated with Pb toxicity, cells from an RD ρ 0 strain (lacking mtDNA) were used.…”

Section: Discussionmentioning

confidence: 99%

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Mitochondria are the main source and one of the targets of Pb (lead)-induced oxidative stress in the yeast Saccharomyces cerevisiae

Sousa

Soares

2014

Appl Microbiol Biotechnol

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The yeast Saccharomyces cerevisiae is a useful model organism for studying lead (Pb) toxicity. Yeast cells of a laboratory S. cerevisiae strain (WT strain) were incubated with Pb concentrations up to 1,000 μmol/l for 3 h. Cells exposed to Pb lost proliferation capacity without damage to the cell membrane, and they accumulated intracellular superoxide anion (O 2 .− ) and hydrogen peroxide (H 2 O 2 ). The involvement of the mitochondrial electron transport chain (ETC) in the generation of reactive oxygen species (ROS) induced by Pb was evaluated. For this purpose, an isogenic derivative ρ 0 strain, lacking mitochondrial DNA, was used. The ρ 0 strain, without respiratory competence, displayed a lower intracellular ROS accumulation and a higher resistance to Pb compared to the WT strain. The kinetic study of ROS generation in yeast cells exposed to Pb showed that the production of O 2 .− precedes the accumulation of H 2 O 2 , which is compatible with the leakage of electrons from the mitochondrial ETC. Yeast cells exposed to Pb displayed mutations at the mitochondrial DNA level. This is most likely a consequence of oxidative stress. In conclusion, mitochondria are an important source of Pb-induced ROS and, simultaneously, one of the targets of its toxicity.

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Section: Discussionmentioning

confidence: 99%

“…This inability to grow on glycerol can be used as a measure of the partial or complete loss of mtDNA (Yazgan and Krebs 2012).…”

Section: Pb-induced Production Of Superoxide Anion and Hydrogen Peroxidementioning

confidence: 99%

Mitochondria are the main source and one of the targets of Pb (lead)-induced oxidative stress in the yeast Saccharomyces cerevisiae

Sousa

Soares

2014

Appl Microbiol Biotechnol

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“…ROS accumulation due to mitochondrial disorder causes destabilization of the mitochondrial and/or nuclear genome. (35,36) BE and its polyphenols effectively suppressed AAPH-induced ROS accumulation in not only cytoplasm but also nuclear (Fig. 4).…”

Section: Discussionmentioning

confidence: 85%

“…(33,34) We previously reported that BE and its component procyanidins and C3G enhanced protein expression of GST family in HepG2 cells. (35) Thus, prevention effect of BE and its polyphenols against ROS accumulation were two ways: a direct radical scavenging activity and inducing GSTs expression indirectly. ROS accumulation due to mitochondrial disorder causes destabilization of the mitochondrial and/or nuclear genome.…”

Section: Discussionmentioning

confidence: 99%

Black soybean seed coat polyphenols prevent AAPH-induced oxidative DNA-damage in HepG2 cells

Yoshioka

Zhang

et al. 2017

J. Clin. Biochem. Nutr.

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Black soybean seed coat extract (BE), which contains abundant polyphenols such as procyanidins, cyanidin 3-glucoside, (+)-catechin, and (−)epicatechin, has been reported on health beneficial functions such as antioxidant activity, anti-inflammatory, anti-obesity, and anti-diabetic activities. In this study, we investigated that prevention of BE and its polyphenols on 2,2'-azobis(2-methylpropionamide) dihydrochloride (AAPH)-induced oxidative DNA damage, and found that these polyphenols inhibited AAPH-induced formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) as a biomarker for oxidative DNA damage in HepG2 cells. Under the same conditions, these polyphenols also inhibited AAPH-induced accumulation of reactive oxygen species (ROS) in the cells. Inhibition of ROS accumulation was observed in both cytosol and nucleus. It was confirmed that these polyphenols inhibited formation of AAPH radical using oxygen radical absorbance capacity assay under the cell-free conditions. These results indicate that polyphenols in BE inhibit free radical-induced oxidative DNA damages by their potent antioxidant activity. Thus, BE is an effective food material for prevention of oxidative stress and oxidative DNA damages.

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“…RD cells are unable to grow on nonfermentable carbon sources, such as glycerol. 55 In a previous work, it was found that the mitochondrion is the main source of intracellular ROS induced by NiO NPs. 19 Because mtDNA is very susceptible to oxidative injury, 56 the possibility of the mitochondrial genome being damaged upon exposure to NiO was evaluated by determining the percentage of RD cells.…”

Section: Impact Of Nio Nps On Cell Viability and Plasmamentioning

confidence: 98%

Nickel Oxide Nanoparticles Trigger Caspase- and Mitochondria-Dependent Apoptosis in the Yeast Saccharomyces cerevisiae

Sousa

Soares

2019

Chem. Res. Toxicol.

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The expansion of the industrial use of nickel oxide (NiO) nanoparticles (NPs) raises concerns about their potential adverse effects. Our work aimed to investigate the mechanisms of toxicity induced by NiO NPs, using the yeast Saccharomyces cerevisiae as a cell model. Yeast cells exposed to NiO NPs exhibited typical hallmarks of regulated cell death (RCD) by apoptosis [loss of cell proliferation capacity (cell viability), exposure of phosphatidylserine at the outer cytoplasmic membrane leaflet, nuclear chromatin condensation, and DNA damage] in a process that required de novo protein synthesis. The execution of yeast cell death induced by NiO NPs is Yca1p metacaspase-dependent. NiO NPs also induced a decrease in the mitochondrial membrane potential and an increase in the frequency of respiratory-deficient mutants, which supports the involvement of mitochondria in the cell death process. Cells deficient in the apoptosis-inducing factor (aif1Δ) displayed higher tolerance to NiO NPs, which reinforces the involvement of mitochondria in RCD by apoptosis. In summary, this study shows that NiO NPs induce caspase-and mitochondria-dependent apoptosis in yeast. Our results warn about the possible harmful effects associated with the use of NiO NPs.

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Mitochondrial and nuclear genomic integrity after oxidative damage in Saccharomyces cerevisiae

Cited by 15 publications

References 108 publications

Mitochondria are the main source and one of the targets of Pb (lead)-induced oxidative stress in the yeast Saccharomyces cerevisiae

Mitochondria are the main source and one of the targets of Pb (lead)-induced oxidative stress in the yeast Saccharomyces cerevisiae

Black soybean seed coat polyphenols prevent AAPH-induced oxidative DNA-damage in HepG2 cells

Nickel Oxide Nanoparticles Trigger Caspase- and Mitochondria-Dependent Apoptosis in the Yeast Saccharomyces cerevisiae

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