Hydrogen peroxide production in yeast cells undergoing programmed cell death in response to acetic acid occurred in the majority of live cells 15 min after death induction and was no longer detectable after 60 min. Superoxide anion production was found later, 60 and 90 min after death induction when cells viability was 60 and 30%, respectively. In cells protected from death due to acid stress adaptation neither hydrogen peroxide nor superoxide anion could be observed after acetic acid treatment. The early production of hydrogen peroxide in cells in which survival was 100% could play a major role in acetic acid-induced programmed cell death signaling. Superoxide anion is assumed to be generated in cells already en route to acetic acid-induced programmed cell death.

• MeSH
• apoptóza fyziologie   MeSH
• katalasa metabolismus   MeSH
• kyselina octová farmakologie   MeSH
• kyseliny farmakologie   MeSH
• peroxid vodíku metabolismus   MeSH
• Saccharomyces cerevisiae enzymologie   fyziologie   MeSH
• superoxiddismutasa metabolismus   MeSH
• superoxidy metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• katalasa MeSH
• kyselina octová MeSH
• kyseliny MeSH
• peroxid vodíku MeSH
• superoxiddismutasa MeSH
• superoxidy MeSH

Superoxide dismutases, both cytosolic Cu, Zn-SOD encoded by SOD1 and mitochondrial Mn-SOD encoded by SOD2, serve Saccharomyces cerevisiae cells for defense against the superoxide radical but the phenotypes of sod1A and sod2delta mutant strains are different. Compared with the parent strain and the sod1delta mutant, the sod2delta mutant shows a much more severe growth defect at elevated salt concentrations, which is partially rescued by 2 mmol/L glutathione. The growth of all three strains is reduced at 37 degrees C, the sod2delta showing the highest sensitivity, especially when cultured in air. Addition of 1 mmol/L glutathione to the medium restores aerobic growth of the sod1delta mutant but has only a minor effect on the growth of the sod2delta strain at 37 degrees C. The sod2delta strain is also sensitive to AsIIl and AsV and its sensitivity is much more pronounced under aerobic conditions. These results suggest that, unlike the Sodlp protein, whose major role is oxidative stress defense, Sod2p also plays a role in protecting S. cerevisiae cells against other stresses--high osmolarity, heat and metalloid stress.

• MeSH
• aerobióza MeSH
• arsen MeSH
• chlorid sodný MeSH
• glutathion farmakologie   MeSH
• kultivační média MeSH
• mitochondrie enzymologie   MeSH
• osmolární koncentrace MeSH
• Saccharomyces cerevisiae - proteiny fyziologie   MeSH
• Saccharomyces cerevisiae účinky léků   fyziologie   MeSH
• superoxiddismutasa 1 MeSH
• superoxiddismutasa fyziologie   MeSH
• vysoká teplota MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• arsen MeSH
• chlorid sodný MeSH
• glutathion MeSH
• kultivační média MeSH
• Saccharomyces cerevisiae - proteiny MeSH
• superoxiddismutasa 1 MeSH
• superoxiddismutasa MeSH
• superoxide dismutase 2 MeSH Prohlížeč

The antioxidative action of amphiphilic mono-(alkanoylamino) ethyldimethylamine-N-oxides (EDA), di-N-oxides 1,1-bis {[2-(N,N-dimethylamino)ethyl]amido}alkane-di-N-oxides (MEDA) and 1,1-bis {[3-(N,N-dimethylamino)propyl]amido}alkane-di-N-oxides (MPDA) with a 12- and 14-membered acyl chain against tert-butylhydroperoxide (TBHP)-produced peroxyl and paraquat (PQ)-generated superoxide radicals was determined in superoxide dismutase-deficient mutants of Saccharomyces cerevisiae, and, in parallel, in a chemical assay based on chemiluminescence changes caused in a luminol system by peroxyl radicals generated from the azo-compound 2,2'-azobis(2-amidinopropane dihydrochloride) (AAPH). At 30 micromol/L, the shorter-chain compounds did not affect strain survival while longer-chain ones, in some cases, lowered the survival of sod2 and sod1 sod2 cells. Whether nontoxic or medium-toxic, all N-oxides protected the sod strains against the toxic effect of PQ and TBHP, the protection being stronger with the di-N-oxides. The survival was lowered only by 14-MPDA in the TBHP-exposed sod2 mutant. Membrane lipids isolated from all strains were protected against TBHP-induced peroxidation by both mono- and di-N-oxides, the protection being dependent on the alkyl chain length. Mono-N-oxides were again less active than di-N-oxides with the same alkyl chains, the antiperoxidative activity being also dependent on lipids isolated from the individual mutants. In the chemiluminescence assay, the IC50 value of the N-oxides for scavenging of radicals generated from AAPH generally decreased (i.e. the scavenging efficiency increased) with increasing chain length and was the highest in MEDA.

• MeSH
• amidiny metabolismus   MeSH
• antioxidancia farmakologie   MeSH
• biotest MeSH
• dimethylaminy chemie   farmakologie   MeSH
• luminiscence MeSH
• luminiscenční měření MeSH
• luminol MeSH
• mutace * MeSH
• oxidancia metabolismus   MeSH
• peroxidy farmakologie   MeSH
• Saccharomyces cerevisiae účinky léků   enzymologie   genetika   fyziologie   MeSH
• scavengery volných radikálů chemie   farmakologie   MeSH
• superoxiddismutasa genetika   MeSH
• terc-butylhydroperoxid farmakologie   MeSH
• Publikační typ
• časopisecké články MeSH
• hodnotící studie MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• 2,2'-azobis(2-amidinopropane) MeSH Prohlížeč
• amidiny MeSH
• antioxidancia MeSH
• dimethylaminy MeSH
• luminol MeSH
• oxidancia MeSH
• perhydroxyl radical MeSH Prohlížeč
• peroxidy MeSH
• scavengery volných radikálů MeSH
• superoxiddismutasa MeSH
• terc-butylhydroperoxid MeSH

Two classes of newly synthesized amphiphilic compounds, phenolic antioxidants ("phenolics") and N-oxides exert in vivo antioxidant effects on live S. cerevisiae cells. Both groups have low toxicity, phenolics being more toxic than N-oxides and compounds with a longer alkyl chain having higher toxicity than those with a shorter alkyl chain. Phenolic antioxidants protect yeast cells exposed to the superoxide producer paraquat and peroxyl generator tert-butylhydroperoxide better than N-oxides at 3-fold higher concentration. Both types of antioxidants enhance the survival of pro-oxidant-exposed cells of S. cerevisiae mutants deficient in cytosolic and/or mitochondrial superoxide dismutase and could be good compounds which mimic the role of superoxide dismutases. The results of measurement of antioxidant activity in an in vitro chemiluminescence test differ from the results obtained in vivo with S. cerevisiae superoxide dismutase mutants. In contrast to their action on live cells, phenolics are less effective than N-oxides in preventing lipid peroxidation of an emulsion of lipids isolated from S. cerevisiae membranes.

• MeSH
• aminy chemie   farmakologie   toxicita   MeSH
• antifungální látky toxicita   MeSH
• antioxidancia chemie   farmakologie   toxicita   MeSH
• delece genu MeSH
• fenoly chemie   farmakologie   toxicita   MeSH
• kvartérní amoniové sloučeniny chemie   farmakologie   toxicita   MeSH
• membránové lipidy metabolismus   MeSH
• mikrobiální viabilita MeSH
• paraquat toxicita   MeSH
• peroxidace lipidů MeSH
• Saccharomyces cerevisiae účinky léků   MeSH
• superoxiddismutasa genetika   MeSH
• terc-butylhydroperoxid toxicita   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• aminy MeSH
• antifungální látky MeSH
• antioxidancia MeSH
• fenoly MeSH
• kvartérní amoniové sloučeniny MeSH
• membránové lipidy MeSH
• paraquat MeSH
• superoxiddismutasa MeSH
• terc-butylhydroperoxid MeSH

Amphiphilic 3-(alkanoylamino)propyldimethylamine-N-oxides with different length of the alkyl chain, i.e. different hydrophilic-lipophilic balance, act in micromolar concentrations as SOD mimics by lifting the inhibition of aerobic growth caused by SOD deletions in Saccharomyces cerevisiae. They also enhance the survival of sod mutants of S. cerevisiae exposed to the hydrophilic superoxide-generating prooxidant paraquat and the amphiphilic hydroperoxide-producing tert-butylhydroperoxide (TBHP), and largely prevent TBHP-induced peroxidation of isolated yeast plasma membrane lipids. Unlike the SOD-mimicking effect, the magnitude of these effects depends on the alkyl chain length of the amine-N-oxides, which incorporate into S. cerevisiae membranes, causing fluidity changes in both the hydrophilic surface part of the membrane and the membrane lipid matrix. Unlike wild-type strains, the membranes of sod mutants were found to contain polyunsaturated fatty acids; the sensitivity of the mutants to lipophilic pro-oxidants was found to increase with increasing content of these acids. sod mutants are useful in assessing pro- and antioxidant properties of different compounds.

• MeSH
• antioxidancia farmakologie   MeSH
• dimethylaminy farmakologie   MeSH
• fluidita membrány účinky léků   MeSH
• membránové lipidy chemie   metabolismus   MeSH
• oxidační stres MeSH
• paraquat toxicita   MeSH
• peroxidace lipidů účinky léků   MeSH
• Saccharomyces cerevisiae účinky léků   enzymologie   MeSH
• superoxiddismutasa chemie   genetika   metabolismus   MeSH
• terc-butylhydroperoxid toxicita   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antioxidancia MeSH
• dimethylaminy MeSH
• membránové lipidy MeSH
• paraquat MeSH
• superoxiddismutasa MeSH
• terc-butylhydroperoxid MeSH

The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSP) as well as of succinate dehydrogenase (SDG), NADH dehydrogenase (NDG) and fumarate hydratase (FHT) were examined in relation to mitochondrial ultrastructure changes in Aspergillus niger exposed to N,N-bis(3-aminopropyl)dodecylamine (Apd) that was shown to exhibit fungicidal activity. There was a progressive increase in SOD, CAT and GSP activities 1 and 4 h after 0.05 and 0.1 % Apd application. However, this was followed by a pronounced activity decrease when 0.05 % Apd treatment was prolonged by 1 d. The destructive effect on fungal morphology was observed when this fungicidal agent was applied at the concentration of 0.1 % for 1 d. In the treated hyphae mitochondria degenerated after all organelles. The morphological malformations of mitochondria had an impact on their metabolic state; however, the activities of SDG, NDG and FHT were affected to a different extent. In A. niger the fungicidal effect of Apd could be mediated by oxidative stress impairing the vital mitochondria-related cellular functions.

• MeSH
• aminy farmakologie   MeSH
• antifungální látky farmakologie   MeSH
• Aspergillus niger účinky léků   metabolismus   ultrastruktura   MeSH
• časové faktory MeSH
• fumarasa metabolismus   MeSH
• glutathionperoxidasa metabolismus   MeSH
• hyfy účinky léků   ultrastruktura   MeSH
• inhibitory enzymů farmakologie   MeSH
• katalasa metabolismus   MeSH
• mitochondrie účinky léků   metabolismus   ultrastruktura   MeSH
• NADH-dehydrogenasa metabolismus   MeSH
• sukcinátdehydrogenasa metabolismus   MeSH
• superoxiddismutasa metabolismus   MeSH
• transmisní elektronová mikroskopie MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• aminy MeSH
• antifungální látky MeSH
• fumarasa MeSH
• glutathionperoxidasa MeSH
• inhibitory enzymů MeSH
• katalasa MeSH
• N,N-bis(3-aminopropyl)dodecylamine MeSH Prohlížeč
• NADH-dehydrogenasa MeSH
• sukcinátdehydrogenasa MeSH
• superoxiddismutasa MeSH

The long-term action of recommended (RC) and near-recommended concentrations of several commercial biocides (Lonzabac 12.100, Genamin CS302D, benzalkonium chloride and 2-phenoxyethanol) on cells of S. cerevisiae wild-type strain DTXII was described using plating tests while short-term effects were determined using the potentiometric fluorescent probe diS-C3(3) that detects both changes in membrane potential and impairment of membrane integrity. A 2-d plating of cells exposed to 0.5xRC of benzalkonium chloride and Genamin CS302D for 15 min showed a complete long-term cell killing, with 2-phenoxyethanol the killing was complete only at 2xRC and Lonzabac caused complete killing at RC but not at 0.5xRC. The diS-C3(3) fluorescence assay performed immediately after a 10-min biocide exposure revealed several concentration-dependent modes of action: Lonzabac at 0.5xRC caused a mere depolarization, higher concentrations causing gradually increasing cell damage; benzalkonium chloride and Genamin CS302D rapidly damaged the membrane of some cells and depolarized the rest whereas 2-phenoxyethanol, which had the lowest effect in the plating test, produced a concentration-dependent fraction of cells with impaired membranes. Cell staining slightly increased during the diS-C3(3) assay; addition of a protonophore showed that part of the remaining undamaged cells retained their membrane potential. Comparison of short-term and long-term data implies that membrane depolarization alone is not sufficient for complete long-term killing of yeast cells under the action of a biocide unless it is accompanied by perceptible impairment of membrane integrity. The results show that the diS-C3(3) fluorescence assay, which reflects the short-term effects of a biocide on cell membranes, can be successfully used to assess the microbicidal efficiency of biocides.

• MeSH
• antiinfekční látky farmakologie   MeSH
• benzalkoniové sloučeniny farmakologie   MeSH
• buněčná membrána účinky léků   MeSH
• ethylenglykoly farmakologie   MeSH
• fluorescenční barviva metabolismus   MeSH
• fluorescenční spektrometrie MeSH
• karbocyaniny metabolismus   MeSH
• membránové potenciály účinky léků   MeSH
• mikrobiální testy citlivosti metody   MeSH
• permeabilita buněčné membrány účinky léků   MeSH
• Saccharomyces cerevisiae účinky léků   růst a vývoj   MeSH
• Publikační typ
• časopisecké články MeSH
• hodnotící studie MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 3,3'-dipropylthiacarbocyanine MeSH Prohlížeč
• antiinfekční látky MeSH
• benzalkoniové sloučeniny MeSH
• ethylenglykoly MeSH
• fluorescenční barviva MeSH
• karbocyaniny MeSH
• phenoxyethanol MeSH Prohlížeč