Effect of superoxide dismutase deficiency on the life span of the yeast Saccharomyces cerevisiae. An oxygen-independent role of Cu,Zn-superoxide dismutase

Wawryn, Jarosław; Święciło, Agata; Bartosz, Grzegorz; Biliński, T

doi:10.1016/s0304-4165(02)00197-6

Cited by 29 publications

(18 citation statements)

References 41 publications

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“…However, oxidized proteins have not been claimed to be responsible for the limited ability of yeast cells to reproduce. Moreover, we (Wawryn et al 2002) and others (Koc et al 2004) did not observe increased replicative lifespan of the yeast cultured under hypoxic and anoxic conditions when oxidative protein damage is attenuated.…”

Section: Introductionmentioning

confidence: 41%

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Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

et al. 2008

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The number of cell divisions of the yeast Saccharomyces cerevisiae is limited, referred to as "replicative lifespan" of this organism and believed to be due to aging mechanisms similar to those of mammalian cells. We demonstrate, using three pairs of isogenic yeast strains (standard and a mutant deficient in an antioxidant defense protein) that although the lifespan differs significantly, the final volume attained after the last division is similar within each pair of strains. In a population, cells cease to bud after various number of cell cycles but attaining a similar final volume. These results indicate that the increase in the mother cell volume, intrinsic to the asymmetric cell division in S. cerevisiae, may be the main mechanism limiting the reproductive capacity of in this organism.

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Section: Introductionmentioning

confidence: 41%

“…The D1CSP4-8C strain is the most long-lived as judged by both these criteria, like its parent strain, SP-4 (Wawryn et al 1997(Wawryn et al , 2002. Maximal lifespan of the BY4741 strain is not much lower but that of the W303-1A strain does not reach 40 buds produced.…”

Section: Resultsmentioning

confidence: 98%

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

et al. 2008

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“…In S. cerevisiae cells, SOD1 accounts for 90-95% of the total SOD activity, and, consequently, a phenotype of the SOD1-depleted mutant (Δsod1) is substantially more pronounced than the SOD2-deleted mutant (Δsod2) (O'Brien et al, 2004;Wawryn, Swieciło, Bartosz, & Biliń ski, 2002). This, in turn, indicates a putative preventive/therapeutic potency of compounds that display antioxidant activity under conditions of improper SOD1 activity.…”

Section: 3mentioning

confidence: 99%

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

Chanaj-Kaczmarek

Wysocki

Karachitos

et al. 2015

Journal of Functional Foods

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“…However, VDAC sensitivity to oxidative modification should not be neglected [e.g., 55]. Accordingly, it has been shown that in the presence of oxidative modification/damage of VDAC the control of the mitochondrial outer membrane permeability might be severely affected leading to mitochondria dysfunction [56][57][58][59]. Moreover, the available data suggest that VDAC isoforms may be differently controlled by oxidative modification of cysteine residues.…”

Section: Vdac As a Versatile Proteinmentioning

confidence: 99%

VDAC as a Potential Target in Huntingtons Disease Therapy: The State of the Art

Karachitos¹,

Grobys²

2015

Pharmaceut Reg Affairs

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It is becoming increasingly evident that mitochondria dysfunction plays an important role in pathogenesis of Huntington's disease (HD). However, the underlying mechanism is still needs to be explained. The crucial aspect of the explanation is to indicate the upstream events in mitochondria dysfunction that could contribute to HD. In the review we propose the defect of voltage-dependent anion-selective channel (VDAC), as a causative event in HDrelated mitochondria dysfunction. Thus, we propose to consider VDAC as a crucial element in HD etiology and consequently as a reasonable target for therapeutic interventions in HD, based on developing novel therapeutic strategies eliminating mitochondria dysfunction.Keywords: Huntington's disease; VDAC; Mitochondria; Therapy Huntington's DiseaseHuntington's disease (HD) is a progressive and fatal neurodegenerative disease with a prevalence of about 5-10/100 000. Clinically, the disease is characterized by progressive chorea (involuntary dance-like movements), rigidity, weight loss, dementia, seizures and psychiatric disturbances such as depression, withdrawal and irritability. These symptoms including cognitive deterioration, psychiatric disturbances, and movement disorders result from a selective and continuous loss of neurons from the striatum and deep layers of the cerebral cortex although other brain regions such as thalamus and subthalamic nucleus are also affected [1][2][3]. Current treatments for HD relieve merely the symptoms and address the control of behavioral symptoms, motor sedatives, cognitive enhancers, and neuroprotective agents [4,5] but are not able to restore neuronal function nor to stop the insidious loss of neurons. As summarized by Kumar et al. [6], although there is an intensive research concerning development of neuroprotective strategies such as fetal neural transplantation, RNA interference (RNAi) and transglutaminase inhibitors (TGaseI), effective therapeutic strategies may not be developed until the next few decades. Thus, a new therapeutic approach involving new potential targets and to start before the symptomatic stage could contribute to HD treatment to be more specific and effective. This, in turn, requires further studies concerning molecular mechanisms underlying HD.The genetic hallmark of HD is an expansion of an unstable trinucleotide CAG repeat region within the first exon of the gene encoding the protein Huntington (Htt). This results in synthesis of its mutant form (mHtt) containing more than 36 glutamine residues at N terminus although the possible contribution of mHtt encoding mRNA, i.e. toxic mRNA in HD etiology has also been suggested [7]. HD inheritance is autosomal dominant and consequently the prevailing view is that mHtt mediated symptoms result from a toxic gain-offunction mechanism although loss-of-function mechanisms for mHtt and Htt are also proposed [8,9]. Htt is conserved among vertebrates [10], is localized mainly in cytoplasm and exhibits anti-apopptotic properties [11,12]. Importantly, Htt expression in diffe...

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Effect of superoxide dismutase deficiency on the life span of the yeast Saccharomyces cerevisiae. An oxygen-independent role of Cu,Zn-superoxide dismutase

Cited by 29 publications

References 41 publications

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

Cell volume as a factor limiting the replicative lifespan of the yeast Saccharomyces cerevisiae

Effects of plant extract antioxidative phenolic compounds on energetic status and viability of Saccharomyces cerevisiae cells undergoing oxidative stress

VDAC as a Potential Target in Huntingtons Disease Therapy: The State of the Art

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