scholarly journals Intracellular pH Homeostasis Plays a Role in the Tolerance of Debaryomyces hansenii and Candida zeylanoides to Acidified Nitrite

2008 ◽  
Vol 74 (15) ◽  
pp. 4835-4840 ◽  
Author(s):  
Henrik Dam Mortensen ◽  
Tomas Jacobsen ◽  
Anette Granly Koch ◽  
Nils Arneborg
Keyword(s):  
Growth Inhibition ◽  
Intracellular Ph ◽  
Yeast Species ◽  
Debaryomyces Hansenii ◽  
Intracellular Acidification ◽  
Plasma Membrane Atpase ◽  
Ph Homeostasis ◽  
Growth Initiation ◽  
The Difference ◽  
Candida Zeylanoides

ABSTRACT The effects of acidified-nitrite stress on the growth initiation and intracellular pH (pHi) of individual cells of Debaryomyces hansenii and Candida zeylanoides were investigated. Our results show that 200 μg/ml of nitrite caused pronounced growth inhibition and intracellular acidification of D. hansenii at an external pH (pHex) value of 4.5 but did not at pHex 5.5. These results indicate that nitrous acid as such plays an important role in the antifungal effect of acidified nitrite. Furthermore, both yeast species experienced severe growth inhibition and a pHi decrease at pHex 4.5, suggesting that at least some of the antifungal effects of acidified nitrite may be due to intracellular acidification. For C. zeylanoides, this phenomenon could be explained in part by the uncoupling effect of energy generation from growth. Debaryomyces hansenii was more tolerant to acidified nitrite at pHex 5.5 than C. zeylanoides, as determined by the rate of growth initiation. In combination with the fact that D. hansenii was able to maintain pHi homeostasis at pHex 5.5 but C. zeylanoides was not, our results suggest that the ability to maintain pHi homeostasis plays a role in the acidified-nitrite tolerance of D. hansenii and C. zeylanoides. Possible mechanisms underlying the different abilities of the two yeast species to maintain their pHi homeostasis during acidified-nitrite stress, comprising the intracellular buffer capacity and the plasma membrane ATPase activity, were investigated, but none of these mechanisms could explain the difference.

Intracellular pH homeostasis plays a role in the NaCl tolerance of Debaryomyces hansenii strains

2005 ◽  
Vol 71 (5) ◽  
pp. 713-719 ◽  
Author(s):  
H. D. Mortensen ◽  
K. Gori ◽  
H. Siegumfeldt ◽  
P. Nissen ◽  
L. Jespersen ◽  
...  
Keyword(s):  
Intracellular Ph ◽  
Debaryomyces Hansenii ◽  
Ph Homeostasis ◽  
Nacl Tolerance

Coupling of Na-H exchange and Na-K pump activity in cultured rat proximal tubule cells

1986 ◽  
Vol 251 (5) ◽  
pp. C815-C824 ◽  
Author(s):  
R. C. Harris ◽  
J. L. Seifter ◽  
C. Lechene
Keyword(s):  
Proximal Tubule ◽  
Intracellular Ph ◽  
Primary Cultures ◽  
Intracellular Acidification ◽  
Ph Homeostasis ◽  
Electron Probe Analysis ◽  
Proximal Tubule Cells ◽  
Pump Activity ◽  
Tubule Cells ◽  
Rat Proximal Tubule

Na-H exchange was studied using electron probe analysis and microfluorescent pH analysis of individual cells, in 3-day primary cultures of rat proximal tubule cells (RPTC) obtained from 40- to 50-day-old Sprague-Dawley rats. After Na-K pump inhibition, the initial rate of net Na influx was inhibited 87% by 1 mM amiloride. K influx, an estimate of Na-K pump activity, was increased approximately three times in cells containing high Na (0.114 mM K X mM P-1 X min-1) compared with control cells containing low Na (0.038 mM K X mM P-1 X min-1). Single cell measurements of RPTC loaded with the cytoplasmic pH indicator 5- (and -6) carboxy-4',5'-dimethylfluorescein indicated that there was reversible intracellular acidification in the absence of external Na or in the presence of amiloride. When intracellular acidification was induced by the addition and subsequent removal of NH4Cl, recovery of intracellular pH was inhibited in the absence of external Na or in the presence of amiloride. Using a similar protocol, it was found that after intracellular acidification, the rate of Na influx increased at least 5.9 times, and intracellular Na content was increased 3.15 +/- 0.64 times at 60 s. There was an initial 50% inhibition of Na-K pump activity within the first 60 s compared with control (nonacidified) RPTC, secondarily followed by an increase in Na-K pump activity. Amiloride (0.5 mM) inhibited the acidification-induced increase in Na influx, and persistent acidification led to a persistent inhibition of Na-K pump activity compared with control. In summary, these results demonstrate that Na-H exchange mediates the majority of net Na influx into RPTC under our basal conditions and is necessary for maintenance of intracellular pH homeostasis. In RPTC, Na-H exchange is further activated by intracellular acidification, leading to a net increase in intracellular Na content, which secondarily stimulates Na-K pump activity. The initial inhibition of Na-K pump activity may be due to a direct effect of intracellular acidification.

Intracellular pH of hepatocytes in primary monolayer culture

1984 ◽  
Vol 246 (5) ◽  
pp. F738-F744 ◽  
Author(s):  
A. S. Pollock
Keyword(s):  
Intracellular Ph ◽  
Monolayer Culture ◽  
Extracellular Ph ◽  
Intracellular Acidification ◽  
Ph Homeostasis ◽  
Distribution Method ◽  
Primary Monolayer Culture ◽  
Primary Monolayer ◽  
Ph Curve ◽  
External Ph

Nonproliferating rat hepatocytes in primary monolayer culture were used for determining liver cell intracellular pH and the degree of intracellular pH homeostasis. The dimethyloxazolidinedione weak acid distribution method was adapted for use in monolayer culture. Intracellular pH of cultured hepatocytes in bicarbonate:CO2 medium was relatively constant at 6.85-7.05 over the external pH range of 7.0-8.0. Below an external pH of 7.0, intracellular pH fell below 6.8. Varying PCO2 between 15 and 40 mmHg did not alter the extracellular versus intracellular pH curve. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid medium, in the absence of bicarbonate, intracellular pH homeostasis was less well defended. In this setting, the intracellular versus extracellular pH relationship curve could be described by a straight line with slope of 0.59 +/- 0.04. The system responded to the addition of the protonophore carbonyl cyanide p-trifluoromethoxyphenyl hydrazone with an increase in the transmembrane pH gradient. Addition of nigericin in 5 mM K+ medium resulted in intracellular acidification to pH 5.5 +/- 0.2. Metabolism of 20 mM added fructose resulted in intracellular acidification. Incubation in sodium-free media at extracellular pH of 7.6 reduced intracellular pH to 6.67 +/- 0.02 compared with an intracellular pH of 6.99 +/- 0.04 in cultures exposed to medium sodium concentrations of 20-80 meq/liter.

Stimulus-evoked changes of extra- and intracellular pH in the leech central nervous system. II. Mechanisms and maintenance of pH homeostasis

1995 ◽  
Vol 73 (1) ◽  
pp. 132-140 ◽  
Author(s):  
C. R. Rose ◽  
J. W. Deitmer
Keyword(s):  
Intracellular Ph ◽  
Complete Suppression ◽  
Gamma Aminobutyric Acid ◽  
Intracellular Acidification ◽  
Ph Homeostasis ◽  
Acid Base ◽  
Bath Application ◽  
Gabaa Receptor Antagonist ◽  
Excitatory Transmitter ◽  
Reversible Reduction

1. We have studied extracellular pH (pHe) and intracellular pH (pHi) changes evoked by repetitive electrical side nerve stimulation (20 Hz, 1 min) in segmental ganglia of the leech Hirudo medicinalis using double-barreled, pH-sensitive microelectrodes to elucidate the involvement of neurotransmitters, of carbonic anhydrase, and of active acid/base transport on the extracellular H+ homeostasis. In saline buffered with 5% CO2-24 mM HCO3-, the stimulation induced a small and brief alkalinization followed by an acidification in the extracellular spaces (ECS), whereas neurons acidified and glial cells alkalinized (see previous paper). 2. Blocking synaptic transmitter release by superfusion with 20 mM Mg2+ saline (CO2/HCO3(-)-free) led to a reversible reduction of both activity-induced pHe changes by approximately 90% and to a complete suppression of the intracellular acidification of neurons. After application of the glutamate/kainate receptor blocker 6-cyano-7-dinitroquinozaline-2,3-dione (CNQX, 50 microM) to CO2/HCO3(-)-free saline, the stimulus-evoked pHe changes were reversibly reduced. The gamma-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin (50 microM) led to an amplification of the extracellular alkalinization in the presence of CO2/HCO3-. Bath application of the excitatory transmitter agonists carbachol or kainate to CO2/HCO3(-)-free saline induced biphasic alkaline-acid transients in the ECS; the inhibitory transmitters GABA and serotonin had no detectable effects on the pHe (saline buffered with CO2/HCO3-).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Biodiversity of yeasts from Illinois maize

1997 ◽  
Vol 43 (4) ◽  
pp. 362-367 ◽  
Author(s):  
M. J. R. Nout ◽  
C. E. Platis ◽  
D. T. Wicklow
Keyword(s):  
Filamentous Fungi ◽  
Debaryomyces Hansenii ◽  
Candida Guilliermondii ◽  
Illinois River ◽  
Trichosporon Cutaneum ◽  
Cryptococcus Albidus ◽  
Candida Shehatae ◽  
Pichia Membranifaciens ◽  
Killer Yeasts ◽  
Candida Zeylanoides

Microflora in wound sites of preharvest maize (including bacteria, yeasts, and filamentous fungi) may play a role in attracting insects to maize plants and may also interact with growth and mycotoxin production by filamentous fungi. As little data are available about the yeasts occurring on maize from the U.S. corn belt, samples of milled maize from experimental plantings at the University of Illinois River Valley Sand Field were analyzed. Yeast counts showed slight yearly fluctuation and varied between 3.60 and 5.88 (log cfu/g maize). The majority of the yeasts were Candida guilliermondii (approximately 55%), Candida zeylanoides (24 %), Candida shehatae (11%), and Debaryomyces hansenii (3%). Also present were Trichosporon cutaneum, Cryptococcus albidus var. aerius, and Pichia membranifaciens. The occurrence of killer yeasts was also evaluated. Killer yeasts were detected in maize for the first time and were identified as Trichosporon cutaneum and Candida zeylanoides. These were able to kill some representative yeasts isolated from maize, including Candida guilliermondii, Candida shehatae, and Cryptococcus albidus var. aerius. Other maize yeasts (Candida zeylanoides, Debaryomyces hansenii, Pichia membranifaciens) were not affected. The majority of yeasts found on maize were unable to ferment its major sugars, i.e., sucrose and maltose. Some (e.g., Candida zeylanoides) were not even able to assimilate these sugars. The importance of these properties in relation to insect attraction to preharvest ears of maize is discussed.Key words: corn, maize, yeast, killer.

Intracellular acidification induces apoptosis by stimulating ICE-like protease activity

1997 ◽  
Vol 110 (5) ◽  
pp. 653-661 ◽  
Author(s):  
I.J. Furlong ◽  
R. Ascaso ◽  
A. Lopez Rivas ◽  
M.K. Collins
Keyword(s):  
Cell Line ◽  
Dna Fragmentation ◽  
Intracellular Ph ◽  
Protease Activity ◽  
Intracellular Acidification ◽  
Over Expression ◽  
Protease Activation ◽  
Dependent Cell ◽  
A Cell ◽  
Ph Decrease

ICE-like protease activation and DNA fragmentation are preceded by a decrease in intracellular pH (pHi) during apoptosis in the IL-3 dependent cell line BAF3. Acidification occurs after 7 hours in cells deprived of IL-3 and after 4 hours when cells are treated with etoposide, close to the time of detection of ICE-like protease activity. Increasing extracellular pH reduces ICE-like protease activation and DNA fragmentation. Bcl-2 over-expression both delays acidification and inhibits ICE-like protease activation. Generation of a rapid intracellular pH decrease, using the ionophore nigericin, induces ICE-like protease activation and apoptosis. ZVAD, a cell permeable inhibitor of ICE-like proteases, does not affect acidification but inhibits apoptosis induced by IL-3 removal or nigericin treatment. These data suggest that intracellular acidification triggers apoptosis by directly or indirectly activating ICE-like proteases.

Intracellular pH homeostasis during cell-cycle progression and growth state transition in Schizosaccharomyces pombe

2001 ◽  
Vol 114 (16) ◽  
pp. 2929-2941 ◽  
Author(s):  
Jim Karagiannis ◽  
Paul G. Young
Keyword(s):  
Cell Cycle ◽  
Schizosaccharomyces Pombe ◽  
Intracellular Ph ◽  
Cell Cycle Progression ◽  
State Transition ◽  
Homeostatic Regulation ◽  
Ph Homeostasis ◽  
Vegetative Cells ◽  
Growth State ◽  
Internal Ph

Accurate measurement of intracellular pH in unperturbed cells is fraught with difficulty. Nevertheless, using a variety of methods, intracellular pH oscillations have been reported to play a regulatory role in the control of the cell cycle in several eukaryotic systems. Here, we examine pH homeostasis in Schizosaccharomyces pombe using a non-perturbing ratiometric pH sensitive GFP reporter. This method allows for accurate intracellular pH measurements in living, entirely undisturbed, logarithmically growing cells. In addition, the use of a flow cell allows internal pH to be monitored in real time during nutritional, or growth state transition. We can find no evidence for cell-cycle-related changes in intracellular pH. By contrast, all data are consistent with a very tight homeostatic regulation of intracellular pH near 7.3 at all points in the cell cycle. Interestingly, pH set point changes are associated with growth state. Spores, as well as vegetative cells starved of either nitrogen, or a carbon source, show a marked reduction in their internal pH compared with logarithmically growing vegetative cells. However, in both cases, homeostatic regulation is maintained.

scholarly journals AE anion exchangers in atrial tumor cells

2001 ◽  
Vol 280 (3) ◽  
pp. H937-H945 ◽  
Author(s):  
Panos Papageorgiou ◽  
Boris E. Shmukler ◽  
Alan K. Stuart-Tilley ◽  
Lianwei Jiang ◽  
Seth L. Alper
Keyword(s):  
Tumor Cell Line ◽  
Disulfonic Acid ◽  
Cell Type ◽  
Intracellular Acidification ◽  
Ph Homeostasis ◽  
Rt Pcr ◽  
Anion Exchangers ◽  
Atrial Tumor ◽  
Atrial Cell ◽  
Exchange Activity

Intracellular pH homeostasis and intracellular Cl−concentration in cardiac myocytes are regulated by anion exchange mechanisms. In physiological extracellular Cl−concentrations, Cl−/HCO[Formula: see text] exchange promotes intracellular acidification and Cl−loading sensitive to inhibition by stilbene disulfonates. We investigated the expression of AE anion exchangers in the AT-1 mouse atrial tumor cell line. Cultured AT-1 cells exhibited a substantial basal Na+-independent Cl−/HCO[Formula: see text] (but not Cl−/OH−) exchange activity that was inhibited by DIDS but not by dibenzamidostilbene disulfonic acid (DBDS). AT-1 cell Cl−/HCO[Formula: see text] activity was stimulated two- to threefold by extracellular ATP and ANG II. AE mRNAs detected by RT-PCR in AT-1 cells included brain AE3 (bAE3), cardiac AE3 (cAE3), AE2a, AE2b, AE2c1, AE2c2, and erythroid AE1 (eAE1), but not kidney AE1 (kAE1). Cultured AT-1 cells expressed AE2, cAE3, and bAE3 polypeptides, which were detected by immunoblot and immunocytochemistry. An AE1-like epitope was detected by immunocytochemistry but not by immunoblot. Both bAE3 and cAE3 were present in intact AT-1 tumors. Cultured AT-1 cells provide a useful system for the study of mediators and regulators of Cl−/HCO[Formula: see text] exchange activity in an atrial cell type.

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