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Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells
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Zeitschriftentitel: | Biochemical Journal |
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Personen und Körperschaften: | , |
In: | Biochemical Journal, 312, 1995, 3, S. 749-756 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Portland Press Ltd.
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Schlagwörter: |
author_facet |
Poulin, R Pegg, A E Poulin, R Pegg, A E |
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author |
Poulin, R Pegg, A E |
spellingShingle |
Poulin, R Pegg, A E Biochemical Journal Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells Cell Biology Molecular Biology Biochemistry |
author_sort |
poulin, r |
spelling |
Poulin, R Pegg, A E 0264-6021 1470-8728 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1042/bj3120749 <jats:p>Polyamines play major roles in ionic and osmotic regulation, but their exact involvement in specific ion transport processes is poorly defined. Treatment of L1210 mouse leukaemia cells with either 5 mM alpha-difluoromethylornithine (DFMO), a suicide substrate of ornithine decarboxylase, or 25 microM N1,N12-bis(ethyl)spermine (BE-3-4-3), a dysfunctional polyamine analogue, caused a stable decreased in intracellular pH (pHi) by 0.1-0.4 unit from steady-state control values between 7.4 and 7.6, as measured either by partition of a weak acid or with a fluorescent pH-sensitive probe. This effect was not related to cell growth status or differences in metabolic acid generation, and was observed in either the presence or absence of HCO3-. Exogenous spermidine (10-25 microM) or putrescine (25-50 microM) fully reversed DFMO- or BE-3-4-3-induced acidification within 2 and 8 h respectively. Recovery of pHi in L1210 cells after a nigericin- or NH4(+)-mediated acid load in HCO3(-)-free buffers was mediated by Na+/H+ antiporter activity, in addition to a minor Na(+)-independent and amiloride-insensitive pathway. Decreased steady-state pHi was maintained in polyamine-depleted L1210 cells after recovery from acid stress. Moreover, the pHi-dependence of the rate of Na(+)-dependent H+ extrusion after an acid stress was altered by DFMO and BE-3-4-3, resulting in a set-point which was lower by 0.25-0.30 pH unit in polyamine-depleted cells. On the other hand, neither the rate nor the magnitude of Na+/H(+)-exchanger-mediated alkalinization induced by hypertonic shock was decreased by polyamine depletion. Thus polyamine depletion induces a persistent defect in pHi homeostasis which is due, at least in part, to a stable decrease in the pHi set-point of the Na+/H+ exchanger.</jats:p> Stable intracellular acidification upon polyamine depletion induced by <i>α</i>-difluoromethylornithine or <i>N</i>1,<i>N</i>12-bis(ethyl)spermine in L1210 leukaemia cells Biochemical Journal |
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1995 |
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Portland Press Ltd. |
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Biochemical Journal |
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title |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_unstemmed |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_full |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_fullStr |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_full_unstemmed |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_short |
Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_sort |
stable intracellular acidification upon polyamine depletion induced by <i>α</i>-difluoromethylornithine or <i>n</i>1,<i>n</i>12-bis(ethyl)spermine in l1210 leukaemia cells |
topic |
Cell Biology Molecular Biology Biochemistry |
url |
http://dx.doi.org/10.1042/bj3120749 |
publishDate |
1995 |
physical |
749-756 |
description |
<jats:p>Polyamines play major roles in ionic and osmotic regulation, but their exact involvement in specific ion transport processes is poorly defined. Treatment of L1210 mouse leukaemia cells with either 5 mM alpha-difluoromethylornithine (DFMO), a suicide substrate of ornithine decarboxylase, or 25 microM N1,N12-bis(ethyl)spermine (BE-3-4-3), a dysfunctional polyamine analogue, caused a stable decreased in intracellular pH (pHi) by 0.1-0.4 unit from steady-state control values between 7.4 and 7.6, as measured either by partition of a weak acid or with a fluorescent pH-sensitive probe. This effect was not related to cell growth status or differences in metabolic acid generation, and was observed in either the presence or absence of HCO3-. Exogenous spermidine (10-25 microM) or putrescine (25-50 microM) fully reversed DFMO- or BE-3-4-3-induced acidification within 2 and 8 h respectively. Recovery of pHi in L1210 cells after a nigericin- or NH4(+)-mediated acid load in HCO3(-)-free buffers was mediated by Na+/H+ antiporter activity, in addition to a minor Na(+)-independent and amiloride-insensitive pathway. Decreased steady-state pHi was maintained in polyamine-depleted L1210 cells after recovery from acid stress. Moreover, the pHi-dependence of the rate of Na(+)-dependent H+ extrusion after an acid stress was altered by DFMO and BE-3-4-3, resulting in a set-point which was lower by 0.25-0.30 pH unit in polyamine-depleted cells. On the other hand, neither the rate nor the magnitude of Na+/H(+)-exchanger-mediated alkalinization induced by hypertonic shock was decreased by polyamine depletion. Thus polyamine depletion induces a persistent defect in pHi homeostasis which is due, at least in part, to a stable decrease in the pHi set-point of the Na+/H+ exchanger.</jats:p> |
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author | Poulin, R, Pegg, A E |
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description | <jats:p>Polyamines play major roles in ionic and osmotic regulation, but their exact involvement in specific ion transport processes is poorly defined. Treatment of L1210 mouse leukaemia cells with either 5 mM alpha-difluoromethylornithine (DFMO), a suicide substrate of ornithine decarboxylase, or 25 microM N1,N12-bis(ethyl)spermine (BE-3-4-3), a dysfunctional polyamine analogue, caused a stable decreased in intracellular pH (pHi) by 0.1-0.4 unit from steady-state control values between 7.4 and 7.6, as measured either by partition of a weak acid or with a fluorescent pH-sensitive probe. This effect was not related to cell growth status or differences in metabolic acid generation, and was observed in either the presence or absence of HCO3-. Exogenous spermidine (10-25 microM) or putrescine (25-50 microM) fully reversed DFMO- or BE-3-4-3-induced acidification within 2 and 8 h respectively. Recovery of pHi in L1210 cells after a nigericin- or NH4(+)-mediated acid load in HCO3(-)-free buffers was mediated by Na+/H+ antiporter activity, in addition to a minor Na(+)-independent and amiloride-insensitive pathway. Decreased steady-state pHi was maintained in polyamine-depleted L1210 cells after recovery from acid stress. Moreover, the pHi-dependence of the rate of Na(+)-dependent H+ extrusion after an acid stress was altered by DFMO and BE-3-4-3, resulting in a set-point which was lower by 0.25-0.30 pH unit in polyamine-depleted cells. On the other hand, neither the rate nor the magnitude of Na+/H(+)-exchanger-mediated alkalinization induced by hypertonic shock was decreased by polyamine depletion. Thus polyamine depletion induces a persistent defect in pHi homeostasis which is due, at least in part, to a stable decrease in the pHi set-point of the Na+/H+ exchanger.</jats:p> |
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spelling | Poulin, R Pegg, A E 0264-6021 1470-8728 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1042/bj3120749 <jats:p>Polyamines play major roles in ionic and osmotic regulation, but their exact involvement in specific ion transport processes is poorly defined. Treatment of L1210 mouse leukaemia cells with either 5 mM alpha-difluoromethylornithine (DFMO), a suicide substrate of ornithine decarboxylase, or 25 microM N1,N12-bis(ethyl)spermine (BE-3-4-3), a dysfunctional polyamine analogue, caused a stable decreased in intracellular pH (pHi) by 0.1-0.4 unit from steady-state control values between 7.4 and 7.6, as measured either by partition of a weak acid or with a fluorescent pH-sensitive probe. This effect was not related to cell growth status or differences in metabolic acid generation, and was observed in either the presence or absence of HCO3-. Exogenous spermidine (10-25 microM) or putrescine (25-50 microM) fully reversed DFMO- or BE-3-4-3-induced acidification within 2 and 8 h respectively. Recovery of pHi in L1210 cells after a nigericin- or NH4(+)-mediated acid load in HCO3(-)-free buffers was mediated by Na+/H+ antiporter activity, in addition to a minor Na(+)-independent and amiloride-insensitive pathway. Decreased steady-state pHi was maintained in polyamine-depleted L1210 cells after recovery from acid stress. Moreover, the pHi-dependence of the rate of Na(+)-dependent H+ extrusion after an acid stress was altered by DFMO and BE-3-4-3, resulting in a set-point which was lower by 0.25-0.30 pH unit in polyamine-depleted cells. On the other hand, neither the rate nor the magnitude of Na+/H(+)-exchanger-mediated alkalinization induced by hypertonic shock was decreased by polyamine depletion. Thus polyamine depletion induces a persistent defect in pHi homeostasis which is due, at least in part, to a stable decrease in the pHi set-point of the Na+/H+ exchanger.</jats:p> Stable intracellular acidification upon polyamine depletion induced by <i>α</i>-difluoromethylornithine or <i>N</i>1,<i>N</i>12-bis(ethyl)spermine in L1210 leukaemia cells Biochemical Journal |
spellingShingle | Poulin, R, Pegg, A E, Biochemical Journal, Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells, Cell Biology, Molecular Biology, Biochemistry |
title | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_full | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_fullStr | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_full_unstemmed | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_short | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
title_sort | stable intracellular acidification upon polyamine depletion induced by <i>α</i>-difluoromethylornithine or <i>n</i>1,<i>n</i>12-bis(ethyl)spermine in l1210 leukaemia cells |
title_unstemmed | Stable intracellular acidification upon polyamine depletion induced by α-difluoromethylornithine or N1,N12-bis(ethyl)spermine in L1210 leukaemia cells |
topic | Cell Biology, Molecular Biology, Biochemistry |
url | http://dx.doi.org/10.1042/bj3120749 |