PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Alkalinity stress”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2004

Characterization of the calcium-mediated response to alkaline stress in Saccharomyces cerevisiae.

Exposure of the yeast Saccharomyces cerevisiae to alkaline stress resulted in adaptive changes that involved remodeling the gene expression. Recent evidence suggested that the calcium-activated protein phosphatase calcineurin could play a role in alkaline stress signaling. By using an aequorin luminescence reporter, we showed that alkaline stress resulted in a sharp and transient rise in cytoplasmic calcium. This increase was largely abolished by addition of EGTA to the medium or in cells lacking Mid1 or Cch1, components of the high affinity cell membrane calcium channel. Under these circumstances, the alkaline response of different calcineurin-sensitive transcriptional promoters was also blocked. Therefore, exposure to alkali resulted in entry of calcium from the external medium, and this triggered a calcineurin-mediated response. The involvement of calcineurin and Crz1/Tcn1, the transcription factor activated by the phosphatase, in the transcriptional response triggered by alkalinization has been globally assessed by DNA microarray analysis in a time course experiment using calcineurin-deficient (cnb1) and crz1 mutants. We found that exposure to pH 8.0 increased at least 2-fold the mRNA levels of 266 genes. In many cases (60%) the response was rather early (peak after 10 min). The transcriptional response of 27 induced genes (10%) was reduced or fully abolished in cnb1 cells. In general, the response of crz1 mutants was similar to that of calcineurin-deficient cells. By analysis of a systematic deletion library, we found 48 genes whose mutation resulted in increased sensitivity to the calcineurin inhibitor FK506. Twenty of these mutations (42%) also provoked alkaline pH sensitivity. In conclusion, our results demonstrated that calcium signaling and calcineurin activation represented a significant component of the yeast response to environmental alkalinization.

Calcium↗
PubMed2006

The transcriptional response of the yeast Na(+)-ATPase ENA1 gene to alkaline stress involves three main signaling pathways.

Adaptive response of the yeast Saccharomyces cerevisiae to environmental alkalinization results in remodeling of gene expression. A key target is the gene ENA1, encoding a Na(+)-ATPase, whose induction by alkaline pH has been shown to involve calcineurin and the Rim101/Nrg1 pathway. Previous functional analysis of the ENA1 promoter revealed a calcineurin-independent pH responsive region (ARR2, 83 nucleotides). We restrict here this response to a small (42 nucleotides) ARR2 5.-region, named MCIR (minimum calcineurin independent response), which contains a MIG element, able to bind Mig1,2 repressors. High pH-induced response driven from this region was largely abolished in snf1 cells and moderately reduced in a rim101 strain. Cells lacking Mig1 or Mig2 repressors had a near wild type response, but the double mutant presented a high level of expression upon alkaline stress. Deletion of NRG1 (but not of NRG2) resulted in increased expression. Induction from the MCIR region was marginal in a quadruple mutant lacking Nrg1,2 and Mig1,2 repressors. In vitro band shift experiments demonstrated binding of Nrg1 to the 5. end of the ARR2 region. Furthermore, we show that Nrg1 binds in vivo around the MCIR region under standard growth conditions, and that binding is largely abolished after high pH stress. Therefore, the calcineurin-independent response of the ENA1 gene is under the regulation of Rim101 (through Nrg1) and Snf1 (through Nrg1 and Mig2). Accordingly, induction by alkaline stress of the entire ENA1 promoter in a snf1 rim101 mutant in the presence of the calcineurin inhibitor FK506 is completely abolished. Thus, the transcriptional response to alkaline stress of the ENA1 gene integrates three different signaling pathways.

Adenosine Triphosphatases↗
PubMed1995

Phenotypically and karyotypically distinct Madin-Darby canine kidney cell clones respond differently to alkaline stress.

We isolated two cell clones from the wild-type Madin-Darby canine kidney cell line (MDCK) that resembles renal collecting duct epithelium. Morphology and karyotypes of the two cell clones were evaluated. The MDCK-C7 cell clone morphologically resembles principal cells (polygonal cell shape, flat), while the MDCK-C11 clone resembles intercalated cells (cuboidal cell shape, high). The diploid chromosome number of MDCK-C7 cells is 83.1 +/- 0.2 (n = 139); that for MDCK-C11 cells is 78.8 +/- 0.1 (n = 128). Culture of MDCK-C7 cells in alkaline medium (pH 7.7) induced irreversible phenotypical and genotypical alterations. Transformed MDCK-C7F cells are characterized by two abnormal (biarmed) chromosomes. In contrast, MDCK-C11 cells are not phenotypically altered by alkaline stress. In order to elucidate the role of intracellular pH (pHi) in the transformation process, we measured pHi under control conditions (pH 7.4), after 5 min exposure to alkaline stress ("acute experiment," pH 7.7) and after incubation of the cells in alkaline medium for two weeks ("chronic experiment," pH 7.7). Under control conditions, MDCK-C7 cells maintained pHi at 7.14 +/- 0.01 (n = 154) and MDCK-C11 cells at 7.01 +/- 0.01 (n = 147). Acute alkaline stress increased pHi of both cell types to similar steady-state values. Under chronic alkaline stress, MDCK-C7 cells were unable to maintain intracellular pH within normal limits exhibiting sustained alkalinization, whereas MDCK-C11 cells could successfully regulate pHi. We conclude that wild-type MDCK cells consist of two genetically distinct subpopulations with different morphology and function. Only the MDCK-C7 clone that resembles the principle cell type of renal collecting duct can be transformed by alkaline stress while the MDCK-C11 clone resists this treatment, due to efficient pHi control mechanisms.

Alkalies↗
PubMed1991

Amine Accumulation in Acidic Vacuoles Protects the Halotolerant Alga Dunaliella salina Against Alkaline Stress.

Amines at alkaline pH induce in cells of the halotolerant alga Dunaliella a transient stress that is manifested by a drop in ATP and an increase of cytoplasmic pH. As much as 300 millimolar NH(4) (+) are taken up by the cells at pH 9. The uptake is not associated with gross changes in volume and is accompanied by K(+) efflux. Most of the amine is not metabolized, and can be released by external acidification. Recovery of the cells from the amine-induced stress occurs within 30 to 60 minutes and is accompanied by massive swelling of vacuoles and by release of the fluorescent dye atebrin from these vacuoles, suggesting that amines are compartmentalized into acidic vacuoles. The time course of ammonia uptake into Dunaliella cells is biphasic-a rapid influx, associated with cytoplasmic alkalinization, followed by a temperature-dependent slow uptake phase, which is correlated with recovery of cellular ATP and cytoplasmic pH. The dependence of amine uptake on external pH indicates that it diffuses into the cells in the free amine form. Studies with lysed cell preparations, in which vacuoles become exposed but retain their capacity to accumulate amines, indicate that the permeability of the vacuolar membrane to amines is much higher than that of the plasma membrane. The results can be retionalized by assuming that the initial amine accumulation, which leads to rapid vacuolar alkalinization, activates metabolic reactions that further increase the capacity of the vacuoles to sequester most of the amine from the cytoplasm. The results indicate that acidic vacuoles in Dunaliella serve as a high-capacity buffering system for amines, and as a safeguard against cytoplasmic alkalinization and uncoupling of photosynthesis.

Journal Article↗
PubMed2003

Bacterial responses to alkaline stress.

Studies of bacterial adaptation to alkaline pH have been less extensive to date compared with those of acidic pH. Recent development of novel methods for global analysis of gene expression under various conditions revealed that many genes were induced at high pH. These data led us to question why so many genes are required for adaptation to alkaline pH. The internal pH of bacteria growing at extremely high pH remains unclear because the methods for measuring interior acidic deltapH developed to date are not so accurate, but it is generally accepted that cytoplasmic pH increases with medium alkalization, although the increase is lower than that of the change in medium pH. Therefore, activities of enzymes working in neutral cytoplasm may decrease with cytoplasmic alkalization under extreme alkaline conditions. Based on these findings, we propose in this article that genes whose products have an optimum activity at high pH are induced under alkaline stress to compensate for the decrease in activities of systems functioning at neutral pH.

Alkalies↗
PubMed2025

Genome-Wide Identification of the TIFY Family in Cannabis sativa L. and Its Potential Functional Analysis in Response to Alkaline Stress and in Cannabinoid Metabolism.

TIFY transcription factors play crucial regulatory roles in secondary metabolism and stress response. However, the expression patterns of the Cannabis sativa L. TIFY gene family under alkali stress, their involvement in cannabinoid metabolism, and their underlying genetic evolutionary mechanisms remain largely unexplored. In this study, we used bioinformatics approaches to conduct genome-wide identification and functional characterization of the C. sativa TIFY gene family. Fourteen TIFY genes were identified and mapped onto seven chromosomes. These genes were classified into four subfamilies: TIFY, JAZ, ZML, and PPD, with the JAZ subfamily further subdivided into five distinct branches. Collinearity analysis suggested that gene duplication events contributed to the expansion of the TIFY gene family in C. sativa. Weighted gene coexpression network analysis (WGCNA) revealed that CsJAZ2, CsJAZ3, and CsJAZ6 participated in the cannabinoid regulatory network. Cis-element analysis indicated that the promoter regions of TIFY genes were enriched in hormone- and stress-responsive elements. Furthermore, transcriptome and RT-qPCR analyses were conducted to examine gene expression patterns under alkaline stress (the RNA employed in RT-qPCR was extracted from the apical leaves of samples subjected to short-duration alkaline stress treatment). The results showed that CsJAZ5 and CsJAZ6 were downregulated, whereas CsPPD1, CsTIFY1, and CsZML1 were upregulated in response to alkali stress. In summary, CsJAZ5, CsPPD1, and CsTIFY1 may serve as candidate genes for the development of alkali-tolerant cultivars, while CsJAZ2 and CsJAZ3 may be valuable targets for enhancing cannabinoid production. This study provides important molecular insights and a theoretical basis for future research on the evolutionary dynamics and functional roles of TIFY transcription factors, particularly in stress adaptation and cannabinoid metabolism.

Cannabis↗
PubMed1991

Alkaline stress transforms Madin-Darby canine kidney cells.

Similar to growth factors aldosterone stimulates Na+/H+ exchange in renal target cells leading to cytoplasmic alkalinization. An alkaline intracellular pH reduces the H+ bonds between repressor proteins and DNA leading to the destabilization of the nuclear chromatin. We observed that sustained alkaline stress "per se" can lead to malignant transformation of Madin-Darby canine kidney (MDCK) cells. Cells grown for two weeks in alkaline culture medium (pH 7.8) developed multiple "foci" composed of spindle-shaped pleomorphic cells lacking contact inhibition and exhibiting poor adhesion to the culture support, typical characteristics of dedifferentiated tumor cells. "Focus" cells were cloned and grown in standard medium (pH 7.4). Cells maintained their abnormal growth pattern, indicating stable pH-induced genetic transformation. Cells were fused with polyethylene glycol to giant cells and impaled with microelectrodes. In contrast to non-transformed giant MDCK cells the plasma membrane potential showed spontaneous oscillations that could be virtually abolished by the omission of extracellular Ca2+ or by the addition of the K+ channel blocker Ba2+. We conclude that sustained alkaline stress can induce malignant transformation in MDCK cells indicated by an abnormal growth pattern and by membrane potential oscillations most likely due to Ca2+ activated K+ channels in the plasma membrane.

Alkalies↗
PubMed2003

Anticipating an alkaline stress through the Tor phosphorelay system in Escherichia coli.

The torCAD operon encoding the TMAO reductase respiratory system is induced in the presence of TMAO by the two-component regulatory system TorS/TorR. The TorS sensor detects TMAO and transphosphorylates the TorR response regulator via a four-step phosphorelay. Once phosphorylated, TorR activates expression of the torCAD structural operon. In order to identify new genes regulated by the Tor regulatory system, we performed a genome-wide transcriptional analysis by using the DNA array technology. We identified seven new transcriptional units whose expression is modulated by the TorS/TorR phosphorelay system. One unit, tnaLAB, is positively regulated whereas the other six, gadA, gadBC, hdeAB, hdeD, yhiE and yhiM, are negatively regulated by this system. Interestingly, the products of some of these units seem to play a role in the survival of E. coli in conditions of extreme pH. The TnaA tryptophanase has been proposed to counteract alkaline stress, whereas the GadA and GadB glutamate decarboxylases and the HdeA and HdeB proteins are involved in the defence against acid stress. Our hypothesis is that the TorS/TorR phosphorelay triggers alkaline-stress defence to limit alkalinization resulting from the reduction of TMAO in alkaline TMA by the Tor respiratory system. The fact that a DeltatnaLAB mutant showed a dramatic decrease in survival as a result of TMAO respiration is in agreement with such a model. As regulation of these genes by the TorS/TorR system does not depend on pH modification but rather on the presence of TMAO, we propose that E. coli anticipates alkalinization of the medium due to TMA production by base-resistance gene activation and acid-resistance gene repression.

Alkalies↗
PubMed2026

Genome-wide identification and characterization of ABC transporters and their expression in response to saline-alkaline stress and WSSV infection in Fenneropenaeus chinensis.

ATP-binding cassette (ABC) transporters play crucial roles in stress responses across organisms, yet their functions in Fenneropenaeus chinensis remain largely unknown. In this study, we identified 42 FcABC genes (FcABCs) in the F. chinensis genome and analyzed their phylogenetic relationships, gene structures, and chromosomal distributions. Phylogenetic analysis grouped the FcABCs into eight subfamilies (ABCA-ABCH), with conserved motif and domain compositions within each subfamily. Expression analysis showed that several FcABC genes, including FcABCG5, FcABCA1, and FcABCC3, were significantly induced under saline-alkaline stress in gill and hepatopancreas tissues. In contrast, most FcABCs were downregulated after WSSV challenge, though a subset (e.g., FcABCB1, FcABCC1) exhibited early upregulation. Functional validation via RNA interference demonstrated that knockdown of FcABCG5 increased shrimp mortality under saline-alkaline stress. Cis-regulatory element analysis revealed an enrichment of stress- and immune-related elements in FcABC promoters. Protein-protein interaction network predictions indicated potential roles for FcABCs in cholesterol metabolism and organic anion transport. Our findings provide insights into the roles of FcABC genes in stress adaptation and immune defense, offering candidate genes for the breeding of stress-resistant shrimp varieties.

Animals↗
PubMed1992

Spontaneous membrane potential oscillations in Madin-Darby canine kidney cells transformed by alkaline stress.

High pH is known to be associated with normal cell growth and neoplastic transformation. We observed that Madin-Darby canine kidney (MDCK) cells grown under sustained alkaline stress (pH 7.7) develop "foci" composed of spindle-shaped cells lacking contact inhibition and exhibiting only poor adhesion to the culture support. Foci-developing (F) cells were cloned and grown in control medium (pH 7.4), where they maintained their neoplastic features indicating a stable pH-induced genetic transformation. After F cells had been fused to giant cells with polyethylene glycol, the cell membrane potential (Vm) was measured by means of microelectrodes. In contrast to non-transformed MDCK cells, Vm of F cells showed spontaneous biorhythmicity caused by periodic opening of Ca2(+)-activated K+ channels. Spiking activity was blunted by the Ca2+ channel blocker nifedipine, by the K+ channel blocker Ba2+, by the Na+/H+ exchange blocker amiloride and its analogue ethylisopropylamiloride, and by an extracellular pH of 7.6 and 6.8. We conclude that MDCK cells transformed by sustained alkaline stress have lost their stable plasma membrane potential but, instead, exhibit endogenous Ca2(+)- and pH-sensitive oscillations.

Animals↗
PubMed1991

Polyphosphate Hydrolysis within Acidic Vacuoles in Response to Amine-Induced Alkaline Stress in the Halotolerant Alga Dunaliella salina.

The location and mobilization of polyphosphates in response to an amine-induced alkaline stress were studied in the halotolerant alga Dunaliella salina. The following observations suggest that polyphosphates accumulate in acidic vacuoles: (a) Accumulation of large amounts of polyphosphates is manifested as intravacuolar dense osmiophilic bodies in electron micrographs. (b) Uptake of amines into the vacuoles induces massive hydrolysis of polyphosphates, demonstrated by in vivo(31)P-nuclear magnetic resonance, and by analysis of hydrolytic products on thin layer chromatograms. The analysis indicates that: (a) Polyphosphate hydrolysis is kinetically correlated with amine accumulation and with the recovery of cytoplasmic pH. (b) The major hydrolytic product is tripolyphosphate. (c) The peak position of the tripolyphosphate terminal phosphate in nuclear magnetic resonance spectra is progressively shifted as the cells recover, indicating that the pH inside the vacuoles increases while the pH in the cytoplasm decreases. (d) In lysed cell preparations, in which vacuoles become exposed to the external pH, mild alkalinization in the absence of amines induces polyphosphate hydrolysis to tripolyphosphates. It is suggested that amine accumulation within vacuoles activates a specific phosphatase, which hydrolyzes long-chain polyphosphates to tripolyphosphates. The hydrolysis increases the capacity of the vacuoles to sequester amines from the cytoplasm probably by releasing protons required to buffer the amine, and leads to recovery of cytoplasmic pH. Thus, polyphosphate hydrolysis provides a high-capacity buffering system that sustains amine compartmentation into vacuoles and protects cytoplasmic pH.

Journal Article↗
PubMed1990

Polyphosphate-hydrolysis--a protective mechanism against alkaline stress?

Different microorganisms, including yeast and algae, accumulate large amounts of polyphosphates. However, the physiological role of polyphosphates is largely unknown. In vivo 31P NMR studies, carried out in the unicellular alga, Dunaliella salina, demonstrate the cytoplasmic alkalization induces massive hydrolysis of polyphosphates, which is correlated kinetically with the recovery of cytoplasmic pH. Analysis of acid extracts of the cells indicates that long-chain polyphosphates are hydrolysed mainly to tripolyphosphate. It is suggested that the hydrolysis of polyphosphates provides a pH-stat mechanism to counterbalance alkaline stress.

Adenosine Triphosphate↗
PubMed1997

Alkaline stress response in Enterococcus faecalis: adaptation, cross-protection, and changes in protein synthesis.

The alkaline shock response in Enterococcus faecalis was studied in this work. Cells adapted to an optimum pH of 10.5 were tolerate to pH 11.9 conditions but acquired sensitivity to acid damage. An analysis of stress proteins revealed that 37 polypeptides were amplified. Two of these are DnaK and GroEL. The combined results show that bile salts and alkaline stress responses are closely related.

Acids↗
PubMed2026

Divergent responses of the gill, hepatopancreas, and eyestalk to acute alkalinity stress in Penaeus vannamei: Osmoregulatory compromise, metabolic trade-off, and endocrine disruption.

The expansion of aquaculture into inland saline-alkali waters is constrained by high carbonate alkalinity (CA), a severe environmental stressor for crustaceans. However, the systemic molecular mechanisms underlying its lethal toxicity remain poorly understood. In this study, we employed a comparative transcriptomic approach to investigate the tissue-specific responses of Pacific white shrimp, Penaeus vannamei, under acute lethal stress (48 h-LC50). We focused on three functionally distinct organs: the gill, hepatopancreas, and eyestalk. The results revealed a systemic but highly tissue-specific transcriptomic response. The gill, as the primary interface, exhibited severe structural impairment and critical failure of osmoregulation, highlighted by the significant downregulation of delta-1-pyrroline-5-carboxylate synthetase (P5CS). In contrast, the hepatopancreas initiates a profound metabolic trade-off, sacrificing growth-related pathways to bolster a robust antioxidant defense system, as evidenced by the activation of sulfur metabolism and high protein turnover. The eyestalk displayed a striking disconnect between hyperactivated stress signaling pathways (e.g., mTOR/FoxO) and the collapse of its protein secretory machinery, marked by the suppression of the ER translocon component Sec61. Collectively, our findings suggest that lethal alkalinity toxicity in P. vannamei results from systemic collapse driven by a complex interplay of osmoregulatory failure, metabolic trade-offs, and endocrine disruption. This study provides a comprehensive molecular snapshot of an organism at its physiological limit, offering novel insights into the adaptive strategies and ultimate tolerance boundaries of crustaceans in extreme environments.

Animals↗
PubMed2002

Cloning and expression of VB12-independent methionine synthase gene responsive to alkaline stress in rice.

VB12-independent methionine synthase is present in higher plants, and catalyzes the methylation of C-homocysteine to form methionine, which is very important for methylation reactions and syntheses of polyamines and ethylene. Under the alkaline condition, using cDNA-RAPD method, a new VB12-independent methionine synthase gene has been cloned and characterized for the first time in rice in this study. The results exhibited that, the cDNA gene entailed 2740 bp, had single copy in the rice genome and encoded peptide of 765 amino acids, the peptide showed 92% and 83% identity with that from Mesembryanthemum cystallinum (U84889) and Cathararanthus roseus (X83499), respectively. It enhanced the transcription more greatly after sodium carbonate treatment for 12 h and 24 h than that of sodium chloride treatment, and then obviously reduced in 48 h later, suggesting that it is related to this stress tolerance in rice.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1996

Exposure of Escherichia coli to acid habituation conditions sensitizes it to alkaline stress.

Escherichia coli transferred from pHo 7.0 to pHo 5.5 or 6.0 became alkali-sensitive by a rapidly induced phenotypic response. Alkali sensitization was reduced at pHo 5.0 and virtually abolished at pHo 6.5. The response was triggered by cytoplasmic rather than external or periplasmic acidification and de novo protein synthesis was needed. Alkali sensitivity failed to appear at pHo 5.5 plus DNA gyrase inhibitors and was markedly reduced by himA, himD, hns, ompC and nhaA lesions. A tonB deletion mutant showed alkali sensitivity at pHo 7.0. Alkali sensitivity induction was not subject to catabolite repression nor was it appreciably affected by a relA lesion. Acid-induced cells were more sensitive to alkali damage to both DNA and beta-galactosidase and to alkali inhibition of beta-galactosidase induction. Alkali sensitization induced at pHo 5.5 may involve NhaB loss.

Alkalies↗
PubMed2005

Alkaline stress-induced apoptosis in human pulmonary artery endothelial cells.

The effect of alkaline stress, or an increase in extracellular pH (pHext), on cell viability is poorly defined. Human pulmonary artery endothelial cells (HPAEC) were subjected to alkaline stress using different methods of increasing pHext. Viability and mode of cell death following alkaline stress were determined by assessing nuclear morphology, ultrastructural features, and caspase-3 activity. Incubation of monolayers in media set to different pHext values (7.4-8.4) for 24-h induced morphological changes suggesting apoptosis (35-45% apoptotic cells) following severe alkaline stress. The magnitude of apoptosis was related to the severity of alkaline stress. These findings were confirmed with an assessment of ultrastructural changes and caspase-3 activation. While there was no difference in the intracellular calcium level ([Ca(2+)](i)) in monolayers set to pHext 7.4 versus 8.4 following the first hour of alkaline stress, blockade of calcium uptake with the chelator, EGTA, potentiated the magnitude of apoptosis under these conditions. Potentiation of apoptosis was reduced by calcium supplementation of the media. Finally, alkaline stress was associated with an increase in intracellular pH. This is the first report of apoptosis following alkaline stress in endothelial cells in the absence of other cell death stimuli.

Apoptosis↗