Antioxidant activity of L-ascorbic acid in wild-type and superoxide dismutase deficient strains of<i>Saccharomyces cerevisiae</i>

Saffi, Jenifer; Sonego, Luciano; Varela, Queli Defaveri; Salvador, Mirian

doi:10.1179/135100006x116691

Cited by 44 publications

(36 citation statements)

References 24 publications

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“…According to Costa et al [40], when wildtype S. cerevisiae is exposed to ethanol-generating superoxide (O 2 •-) and H 2 O 2 during both diauxic and post-diauxic growth and the mitochondrial Sod mutant (Sod2∆) produces essential protection against oxidative stress. A similar study was suggested while working on L-ascorbic acid by Saffi et al [41]. In this study, both formulations of PYT protected the cytosolic Sod1∆, mitochondrial Sod2∆, and liver Cat1∆ mutants, which may confirm the potential protection against oxidative damage by PYT.…”

Section: Study-based Conclusive Talkssupporting

confidence: 64%

Preparation of phytol-loaded nanoemulsion and screening for antioxidant capacity

Islam

Streck²,

Paz³

et al. 2016

Int Arch Med

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The study prepared a nanoemulsion with a diterpenoid isoprenoid alcohol called phytol (PYT) and subsequently tested it for antioxidant capacity. For this, PYT-loaded nanoemulsion was prepared by phase inversion method and both PYT-containing nanoemulsion (PNE) and PYT-free nanoemulsion (PFNE) (2-16 µM) were tested for antiradical activity (DPPH•: 1,1-dipheny-picrylhydrazyl radical; ABTS•+: azino-bisethylbenzthiazoline-sulfonic acid; •OH: hydroxyl radical scavenging; NO•: nitrite oxide radical), lipid peroxidation (LP), reduction potential (RP), and inhibition of hemolysis (HL) in rat erythrocytes in comparison with an α-tocopherol analogue (Trolox -TRO -positive control). In addition, an in vivo test was performed with wildtype and deficient Saccharomyces cerevisiae strains using hydrogen peroxide (H 2 O 2 ) as a stressor. Results suggest that PNE exhibited higher antioxidant than the PFNE. Increasing doses reveled antioxidant capacity in a dose-dependent manner. In the S. cerevisiae study, both PFNEand PNE-treated groups exhibited decreased rates of survival with the highest doses, whichever in the presence of stressor increased the survival rates, which indicates antioxidative defense capacity of PYT. In this occasion, PNE exhibited prominent antioxidative defense in the presence of stressor rather than PFNE. In conclusion, PYT exhibited potential antioxidant activity but at high concentration it was toxic to the yeast cells. The production of PYT-nanoemulsions may be relevant to the pharmaceutical sciences.

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Section: Study-based Conclusive Talkssupporting

confidence: 64%

Preparation of phytol-loaded nanoemulsion and screening for antioxidant capacity

Islam

Streck²,

Paz³

et al. 2016

Int Arch Med

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“…About genes related to oxidative stress, ScHap1p is required for full SOD2 aerobic expression and the DNA sequences necessary for repression in the absence of heme overlap those that mediate Hap1p activation (Pinkham et al, 1997). SOD2 encodes for a mitochondrial superoxide dismutase that protects cells against oxygen toxicity (Saffi et al, 2006;van Loon et al, 1986). Besides, deletion of ScHAP1 led to a 50% reduction of TSA2 transcriptional activity and it was reported that heme stimulated TSA2 transcription by activating ScHap1p (Wong et al, 2002).…”

Section: In Aerobic Conditions Transcriptional Control Mediated Bymentioning

confidence: 98%

Functional characterization of KlHAP1: A model to foresee different mechanisms of transcriptional regulation by Hap1p in yeasts

Lamas-Maceiras

Núñez

Rodrı́guez-Belmonte

et al. 2007

Gene

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“…These findings support a role for CL in Fe-S cluster formation and/or transfer of Fe-S clusters to apoproteins. crd1⌬ was also synthetically lethal with a mutant in SOD2, which codes for mitochondrial manganese superoxide dismutase, an enzyme that protects cells against oxygen toxicity (38,39). Disruption of SOD2 in the CL mutant may lead to lethality due to severe oxidative stress or accumulation of free radicals.…”

Section: Go Termmentioning

confidence: 99%

Loss of Cardiolipin Leads to Perturbation of Acetyl-CoA Synthesis

Raja

Joshi

et al. 2017

Journal of Biological Chemistry

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Edited by George M. CarmanCardiolipin (CL), the signature phospholipid of mitochondrial membranes, plays an important role in mitochondrial processes and bioenergetics. CL is synthesized de novo and undergoes remodeling in the mitochondrial membranes. Perturbation of CL remodeling leads to the rare X-linked genetic disorder Barth syndrome, which shows disparities in clinical presentation. To uncover biochemical modifiers that exacerbate CL deficiency, we carried out a synthetic genetic array screen to identify synthetic lethal interactions with the yeast CL synthase mutant crd1⌬. The results indicated that crd1⌬ is synthetically lethal with mutants in pyruvate dehydrogenase (PDH), which catalyzes the conversion of pyruvate to acetyl-CoA. Acetyl-CoA levels were decreased in the mutant. The synthesis of acetylCoA depends primarily on the PDH-catalyzed conversion of pyruvate in the mitochondria and on the PDH bypass in the cytosol, which synthesizes acetyl-CoA from acetate. Consistent with perturbation of the PDH bypass, crd1⌬ cells grown on acetate as the sole carbon source exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels resulting from decreased acetyl-CoA synthetase activity. PDH mRNA and protein levels were up-regulated in crd1⌬ cells, but PDH enzyme activity was not increased, indicating that PDH up-regulation did not compensate for defects in the PDH bypass. These findings demonstrate for the first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient cells as a result of a defective PDH bypass pathway. Cardiolipin (CL)4 is a unique phospholipid with dimeric structure that constitutes about 15% of the total phospholipid in mitochondria (1-4). CL is synthesized de novo in the inner mitochondrial membrane (5) and undergoes remodeling in which saturated fatty acyl chains are replaced with unsaturated fatty acids (6, 7). CL plays an important role in maintenance of mitochondrial structure, interaction with mitochondrial membrane proteins, respiration and stability of respiratory chain supercomplexes (8 -10), and other mitochondrial functions such as protein import and maintenance of the membrane potential (11-13). Loss of CL perturbs mitochondrial bioenergetics and decreases ATP synthesis (12, 14 -16). Aberrant CL remodeling due to mutation of tafazzin, the transacylase that remodels CL, leads to the severe genetic disorder Barth syndrome (BTHS) (17). Loss of tafazzin results in decreased total CL, increased monolysocardiolipin, and aberrant CL species (18 -20). In yeast, tafazzin mutant phenotypes are not due to aberrant CL species but more likely result from decreased total CL/increased monolysocardiolipin (21, 22). The clinical presentation of BTHS includes cardio-and skeletal myopathy, neutropenia, 3-methylglutaconic aciduria, growth retardation, abnormal mitochondria, and defective oxidative phosphorylation (23). However, disparities in the clinical manifestation are characteristic of the disorder (24 -26), indicating that physiologi...

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Antioxidant activity of L-ascorbic acid in wild-type and superoxide dismutase deficient strains ofSaccharomyces cerevisiae

Cited by 44 publications

References 24 publications

Preparation of phytol-loaded nanoemulsion and screening for antioxidant capacity

Preparation of phytol-loaded nanoemulsion and screening for antioxidant capacity

Functional characterization of KlHAP1: A model to foresee different mechanisms of transcriptional regulation by Hap1p in yeasts

Loss of Cardiolipin Leads to Perturbation of Acetyl-CoA Synthesis

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