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  • Na+/H+ exchange  (2)
  • leukocytes  (1)
  • nigericin  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Bioscience reports 8 (1988), S. 65-76 
    ISSN: 1573-4935
    Keywords: amiloride ; Na+/H+ exchange ; antiport ; superoxide ; leukocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The cytoplasmic pH undergoes a biphasic change when neutrophils are activated. The role of Ca2+ in initiating these changes was investigated. No correlation was found between the increased cytosolic [Ca2+] and the stimulation of the Na+/H+ antiport. Similarly, the cytoplasmic acidification elicited by activation in Na+-free media was found to be unrelated to [Ca2+]. Reversal of Na+/H+ exchange was also ruled out as the source of the acidification. Data using a variety of soluble activators indicate that metabolic acid generation is largely responsible for the observed drop in cytoplasmic pH.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 116 (1990), S. 139-148 
    ISSN: 1432-1424
    Keywords: intracellular pH ; cytoplasmic Ca2+ ; thymic lymphocytes ; chelator ; trace metals ; nigericin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effect of lowering intracellular pH on the membrane potential (E m ) of rat thymic lymphocytes was studied using the potential-sensitive dyebis-oxonol. Cells were acid loaded by addition of the electroneutral K+/H+ exchanging ionophore nigericin. Acidification to pH 6.3 in Na+-free solution resulted in a biphasic change inE m : an early transient hyperpolarization followed by a sustained depolarization. These changes were associated with a rise in cytosolic free Ca2+ ([Ca2+] i ). The hyperpolarization was eliminated when the change in [Ca2+] i was prevented using BAPTA, an intracellular Ca2+ chelator. Moreover, a similar hyperpolarization was elicited by elevation of [Ca2+] i at physiological pH i using ionomycin, suggesting involvement of Ca2+-activated K+ channels. In contrast, the depolarization phase could not be mimicked by raising [Ca2+] i with ionomycin. However, intracellular BAPTA effectively inhibited the acidificationinduced depolarization. Inhibition was also obtained by extracellular addition of EGTA or dithiothreitol, even when the external free Ca2+ concentration remained unaltered. These observations suggested a possible role of contaminating trace metals. Cytosolic acidification is envisaged to induce intracellular accumulation of one or more trace metals, which induces the observed changes inE m . Accordingly, similar changes inE m can be induced without acidification by the addition of small amounts of Cu2+ to the medium. The ionic basis of theE m changes induced by acidification and the significance of these observations are discussed.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bioenergetics and biomembranes 29 (1997), S. 393-399 
    ISSN: 1573-6881
    Keywords: Na+/H+ exchange ; proton pump ; V-ATPase ; anion exchange ; cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Both cellular proliferation and apoptosis (programmed cell death) have been claimed to be modulated, perhaps even triggered by, changes in intracellular pH. In this review, we summarize the evidence that gave rise to these hypotheses. To facilitate a critical appraisal of the existing data, we briefly review the main pathways involved in cytosolic pH homeostasis and their regulation by mitogens and by apoptosis-inducing agents. The information available at present suggests that cytosolic pH plays a permissive role in cellular growth and proliferation, but is neither a trigger nor an essential step in the mitogenic signal transduction cascade. Concerning apoptosis, it is clear that lowering the pH in vitro can activate DNase II. However, the evidence linking cytosolic acidification with DNA degradation in vivois presently not convincing. We conclude that the cytosolic pH, an essential physiological parameter that is tightly controlled by multiple, complementary, or redundant systems, is unlikely to play a role in signalling either cell growth or death.
    Type of Medium: Electronic Resource
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