Yeast lacking superoxide dismutase. Isolation of genetic suppressors.

Liu, X.F.; Elashvili, Ilya; Gralla, Edith Butler; Valentine, Joan Selverstone; Lapinskas, Paula J.; Culotta, Valeria C.

doi:10.1016/s0021-9258(19)36959-5

Cited by 139 publications

(10 citation statements)

References 30 publications

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“…Evaluation of Antioxidant Capacity Using Yeast Cells. The evaluation of the in vivo antioxidant actitivity of hesperidin was performed using SOD proficient and deficient S. cerevisiae yeast strains ( Table ), which were kindly provided by Dr. E. Gralla from University of California, Los Angeles, CA ( , ). The flavonoid hesperidin was prepared with a 10 mM solution in DMSO immediately prior to use.…”

Section: Methodsmentioning

confidence: 99%

Antioxidant Activity of the Flavonoid Hesperidin in Chemical and Biological Systems

Wilmsen

Spada

Salvador

2005

J. Agric. Food Chem.

260

161

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The antioxidant hesperidin, a major flavonoid in sweet orange and lemon, was evaluated using chemical and biological systems. The chemical assay evaluates the hesperidin capacity to sequester 1,1-diphenyl-2-picrylhydrazyl (DPPH*). Biological studies were done using the eukaryotic cells of superoxide-dismutase proficient and deficient strains of Saccharomyces cerevisiae treated with hesperidin and the stressing agents hydrogen peroxide or paraquat (methylviologen; 1,1'-dimethyl-4,4'-bipyridinium dichloride). Hesperidin was able to reduce significantly the level of the free radical DPPH* with similar efficacy of trolox (positive control). When the yeast cells were exposed to the flavonoid hesperidin before the stressing agents, there was a significant increase in the survival of all strains. Paraquat induced higher catalase and superoxide dismutase than did hydrogen peroxide, which only increased catalase activity. Previous addition of hesperidin to these treatments was able to reduce significantly both enzymatic levels. These observations clearly demonstrate that hesperidin provides strong cellular antioxidant protection against the damaging effects induced by paraquat and peroxide hydrogen.

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Section: Methodsmentioning

confidence: 99%

Antioxidant Activity of the Flavonoid Hesperidin in Chemical and Biological Systems

Wilmsen

Spada

Salvador

2005

J. Agric. Food Chem.

260

161

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“…Mutant strains of Saccharomyces cereVisiae are described in Table 1. The sod1 null mutation (sod1∆::URA3) was introduced into EG103 to generate EG119 and CC118 as previously described (Liu et al, 1992). To determine the relative percentage of Q 6 H 2 present in sod mutant strains, yeast were grown in 100 mL of liquid cultures of 1% bacto yeast extract, 2% bacto peptone, and either 2% dextrose, glycerol, ethanol, or lactate at 30 °C overnight (YPD) to an OD 600 12-18 or for 2 days (YPG, YPE, YPL) to an OD 600 1.0-1.5.…”

Section: Methodsmentioning

confidence: 99%

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

et al. 1996

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Ubiquinone (Q) is an essential, lipid soluble, redox component of the mitochondrial respiratory chain. Much evidence suggests that ubiquinol (QH 2 ) functions as an effective antioxidant in a number of membrane and biological systems by preventing peroxidative damage to lipids. It has been proposed that superoxide dismutase (SOD) may protect QH 2 from autoxidation by acting either directly as a superoxide-semiquinone oxidoreductase or indirectly by scavenging superoxide. In this study, such an interaction between QH 2 and SOD was tested by monitoring the fluorescence of cis-parinaric acid (cPN) incorporated phosphatidylcholine (PC) liposomes. Q 6 H 2 was found to prevent both fluorescence decay and generation of lipid peroxides (LOOH) when peroxidation was initiated by the lipid-soluble azo initiator DAMP, dimethyl 2,2′-azobis (2-methylpropionate), while Q 6 or SOD alone had no inhibitory effect. Addition of either SOD or catalase to Q 6 H 2 -containing liposomes had little effect on the rate of peroxidation even when incubated in 100% O 2 . Hence, the autoxidation of QH 2 is a competing reaction that reduces the effectiveness of QH 2 as an antioxidant and was not slowed by either SOD or catalase. The in ViVo interaction of SOD and QH 2 was also tested by employing yeast mutant strains harboring deletions in either CuZnSOD and/or MnSOD. The sod mutant yeast strains contained the same percent Q 6 H 2 per cell as wild-type cells. These results indicate that the autoxidation of QH 2 is independent of SOD.

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“…Strains of S. cerevisiae used in these studies are the following: EG103 (wild type) (DBY746; MAT ␣ leu2-3,112 his3 ⌬ 1 trp1-289 ura3-52 GAL ϩ ), EG118 ( sod1 ⌬ ) (EG103 with sod1 ⌬ A::URA3 ), and EG133 ( sod1 ⌬ sod2 ⌬ ) (EG103 with sod1 ⌬ A::URA3 sod2 ⌬ ::TRP1 ) (9,23). In these strains the mutations in SOD1 and SOD2 are deletions of most of the coding region.…”

Section: Yeast Strainsmentioning

confidence: 99%

“…Culotta and co-workers (21)(22)(23) have recently identified several mutations that partially "rescue" the sod1⌬ sod2⌬ strain, and they showed that each of these mutations altered copper or manganese metabolism in some way. One of these, the pmr1 mutation, exerted its effects by increasing cellular manganese accumulation.…”

Section: Effects Of Bcl-2 Are Not Due To Altered Copper or Manganese Metabolismmentioning

confidence: 99%

Human Bcl-2 Reverses Survival Defects in Yeast Lacking Superoxide Dismutase and Delays Death of Wild-Type Yeast

Longo

Ellerby

Bredesen

et al. 1997

The Journal of Cell Biology

195

124

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We expressed the human anti-apoptotic protein, Bcl-2, in Saccharomyces cerevisiae to investigate its effects on antioxidant protection and stationary phase survival. Yeast lacking copper-zinc superoxide dismutase (sod1Δ) show a profound defect in entry into and survival during stationary phase even under conditions optimal for survival of wild-type strains (incubation in water after stationary phase is reached). Expression of Bcl-2 in the sod1Δ strain caused a large improvement in viability at entry into stationary phase, as well as increased resistance to 100% oxygen and increased catalase activity. In addition, Bcl-2 expression reduced mutation frequency in both wild-type and sod1Δ strains. In another set of experiments, wild-type yeast incubated in expired minimal medium instead of water lost viability quickly; expression of Bcl-2 significantly delayed this stationary phase death. Our results demonstrate that Bcl-2 has activities in yeast that are similar to activities it is known to possess in mammalian cells: (a) stimulation of antioxidant protection and (b) delay of processes leading to cell death.

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Yeast lacking superoxide dismutase. Isolation of genetic suppressors.

Cited by 139 publications

References 30 publications

Antioxidant Activity of the Flavonoid Hesperidin in Chemical and Biological Systems

Antioxidant Activity of the Flavonoid Hesperidin in Chemical and Biological Systems

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

Human Bcl-2 Reverses Survival Defects in Yeast Lacking Superoxide Dismutase and Delays Death of Wild-Type Yeast

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