Hydrogen peroxide-induced response in E. coli and S. cerevisiae: different stages of the flow of the genetic information

Semchyshyn, Halyna M.

doi:10.2478/s11535-009-0005-5

Cited by 23 publications

(32 citation statements)

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“…Earlier we suggested that cells treated with low sublethal concentrations of hydrogen peroxide accumulated non-active stress-protective molecules, further activation of which made microorganisms resistant to lethal concentrations of H 2 O 2 . 25,47 Overall, microorganism exposure to mild stress leads to the acquisition of cellular resistance to lethal stress. 5,6,[23][24][25] Here we found that H 2 O 2 pre-incubation increased the survival of yeast exposed to 200 mM AA (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…For example, yeast exposed to a mild dose of oxidative stress could subsequently survive an otherwise lethal dose of the same or another stress. 5,6,[23][24][25] The latter is known as 'cross-adaptation' or 'cross-protection'. In the present work, we examined the influence of cell pre-adaptation by sublethal concentrations of hydrogen peroxide on yeast survival under acid stress.…”

Section: Introductionmentioning

confidence: 99%

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Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

et al. 2011

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The influence of acetic and propionic acids on baker's yeast was investigated in order to expand our understanding of the effect of weak organic acid food preservatives on eukaryotic cells. Both acids decreased yeast survival in a concentration-dependent manner, but with different efficiencies. The acids inhibited the fluorescein efflux from yeast cells. The inhibition constant of fluorescein extrusion from cells treated with acetate was significantly lower in parental strain than in either PDR12 (ABC-transporter Pdr12p) or WAR1 (transcriptional factor of Pdr12p) defective mutants. The constants of inhibition by propionate were virtually the same in all strains used. Yeast exposure to acetate increased the level of oxidized proteins and the activity of antioxidant enzymes, while propionate did not change these parameters. This suggests that various mechanisms underlie the yeast toxicity by acetic and propionic acids. Our studies with mutant cells clearly indicated the involvement of Yap1p transcriptional regulator and de novo protein synthesis in superoxide dismutase up-regulation by acetate. The up-regulation of catalase was Yap1p independent. Yeast pre-incubation with low concentrations of H 2 O 2 caused cellular cross-protection against high concentrations of acetate. The results are discussed from the point of view that acetate induces a prooxidant effect in vivo, whereas propionate does not.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

et al. 2011

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“…Ectopic application of sublethal concentrations of H 2 O 2 in budding yeast induces the transcription of genes encoding both the cytosolic Cu/Zn-dependent and the mitochondrial Mn-dependent superoxide dismutases SOD1 and SOD2 (13,14) as well as an increase in levels of the corresponding proteins (13 also induces transcription of the superoxide dismutase sodA in Escherichia coli (15) and the transcription and activity of MnSOD, but not Cu/Zn-SOD in rat cells (16). To determine whether induction of Sod1p and/or Sod2p activity underlies the reduction in O 2 − levels that accompanies increases in intracellular H 2 O 2 , we measured the activities of Sod1p and Sod2p under CR and non-CR conditions in wild-type and CTA1 mutant cells.…”

Section: Elevated H 2 O 2 Levels Induced By Cr or Inactivation Of Catmentioning

confidence: 99%

Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H ₂ O ₂ and superoxide dismutase activity

Mesquita

Weinberger²,

Silva³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

248

227

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The free radical theory of aging posits oxidative damage to macromolecules as a primary determinant of lifespan. Recent studies challenge this theory by demonstrating that in some cases, longevity is enhanced by inactivation of oxidative stress defenses or is correlated with increased, rather than decreased reactive oxygen species and oxidative damage. Here we show that, in Saccharomyces cerevisiae, caloric restriction or inactivation of catalases extends chronological lifespan by inducing elevated levels of the reactive oxygen species hydrogen peroxide, which activate superoxide dismutases that inhibit the accumulation of superoxide anions. Increased hydrogen peroxide in catalase-deficient cells extends chronological lifespan despite parallel increases in oxidative damage. These findings establish a role for hormesis effects of hydrogen peroxide in promoting longevity that have broad implications for understanding aging and age-related diseases.aging | hydrogen peroxide | hormesis | antioxidant enzymes | oxidative damage T he longstanding free radical theory has guided investigations into the causes and consequences of aging for more than 50 y (1). However, the results of a number of recent studies have failed to provide support for the free radical theory or suggest that this theory is at best incomplete (2). Studies of naked mole rats, for example, demonstrated that this extremely long-lived rodent exhibits high levels of oxidative damage compared with mice or rats, whose lifespans are ≈1/10 that of naked mole rats (3). In addition, caloric restriction (CR), which extends the lifespans of a variety of eukaryotic organisms, promotes longevity in Caenorhabditis elegans by a mechanism that involves increased oxidative stress (4). In fact, in contrast to the destructive effects of reactive oxygen species (ROS), recent evidence indicates that in mammals, hydrogen peroxide (H 2 O 2 ) and other forms of ROS function as essential secondary messengers in the regulation of a variety of physiological processes (reviewed in ref. 5). For example, H 2 O 2 activates prosurvival signaling pathways mediated by p53, NF-κB, AP-1, and other molecules (6). Furthermore, increases in the intracellular steady-state production of H 2 O 2 by SOD2 overexpression can block the activation of cellular processes required for programmed cell death (7). However, a causal relationship between CR and effects on oxidative stress has been difficult to establish.To better understand how CR impacts oxidative stress and longevity in the model organism Saccharomyces cerevisiae, in this study we examined intracellular levels of H 2 O 2 and superoxide anions (O 2 − ), which are two forms of ROS implicated in aging in all eukaryotes, under CR and other conditions. Our findings indicate that CR or inactivation of catalases extends chronological lifespan (CLS) by inducing elevated levels of H 2 O 2 , which activate superoxide dismutases that inhibit the accumulation of O 2 − . These findings establish a role for hormesis effects of H 2 O 2 in promoting l...

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“…Specific mechanisms may differ substantially, but a decrease in the activity is a common event. Increases in the activities of antioxidant and associated enzymes under oxidative stress are usually connected with their de novo synthesis [29,35] or activation of preexisting inactive molecules [5,6,52]. Although activation of inactive enzyme molecules is still debatable issue, up-regulation of their biosynthesis is well-established.…”

Section: Fig 2 Relationships Between the Dose Of An Inducer Of Oxidmentioning

confidence: 99%

Intensity - and Time Course-Based Classifications of Oxidative Stresses

Lushchak

2015

jpnu

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Abstract. In living organisms, production of reactive oxygen species (ROS) is counterbalanced by their elimination and/or prevention of formation which in concert can typically maintain a steadystate (stationary) ROS level. However, this balance may be disturbed and lead to elevated ROS levels and enhanced damage to biomolecules. Since 1985, when H. Sies first introduced the definition of oxidative stress, this area has become one of the hot topics in biology and, to date, many details related to ROS-induced damage to cellular components, ROS-based signaling, cellular responses and adaptation have been disclosed. However, some basal oxidative damage always occurs under unstressed conditions, and in many experimental studies it is difficult to show definitely that oxidative stress is indeed induced by the stressor. Therefore, usually researchers experience substantial difficulties in the correct interpretation of oxidative stress development. For example, in many cases an increase or decrease in the activity of antioxidant and related enzymes are interpreted as evidences of oxidative stress. Careful selection of specific biomarkers (ROSmodified targets) may be very helpful. To avoid these sorts of problems, I propose several classifications of oxidative stress based on its time-course and intensity. The time-course classification includes acute and chronic stresses. In the intensity based classification, I propose to discriminate four zones of function in the relationship between "Dose/concentration of inducer" and the measured "Endpoint": I -basal oxidative stress zone (BOS); II -low intensity oxidative stress (LOS); III -intermediate intensity oxidative stress (IOS); IV -high intensity oxidative stress (HOS). The proposed classifications may be helpful to describe experimental data where oxidative stress is induced and systematize it based on its time course and intensity. Perspective directions of investigations in the field include development of sophisticated classifications of oxidative stresses, accurate identification of cellular ROS targets and their arranged responses to ROS influence, real in situ functions and operation of so-called "antioxidants", intracellular spatiotemporal distribution and effects of ROS, deciphering of molecular mechanisms responsible for cellular response to ROS attacks, and ROS involvement in realization of normal cellular functions in cellular homeostasis.

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Hydrogen peroxide-induced response in E. coli and S. cerevisiae: different stages of the flow of the genetic information

Cited by 23 publications

References 89 publications

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H ₂ O ₂ and superoxide dismutase activity

Intensity - and Time Course-Based Classifications of Oxidative Stresses

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Hydrogen peroxide-induced response in E. coli and S. cerevisiae: different stages of the flow of the genetic information

Cited by 23 publications

References 89 publications

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Acetate but not propionate induces oxidative stress in bakers’ yeastSaccharomyces cerevisiae

Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H 2 O 2 and superoxide dismutase activity

Intensity - and Time Course-Based Classifications of Oxidative Stresses

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Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H ₂ O ₂ and superoxide dismutase activity