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Difference between revisions of "Kwast 1995 BBA"

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{{Publication
{{Publication
|title=Kwast KE, Shapiro JI, Rees BB, Hand SC (1995) Oxidative phosphorylation and the realkanization of intracellular pH during recovery from anoxia in Artemia franciscana embryos. Biochim. Biophys. Acta 1232: 5-12.
|title=Kwast KE, Shapiro JI, Rees BB, Hand SC (1995) Oxidative phosphorylation and the realkanization of intracellular pH during recovery from anoxia in Artemia franciscana embryos. Biochim Biophys Acta 1232:5-12.
|info=[http://www.sciencedirect.com/science/article/pii/0005272895000909 ScienceDirect]
|info=[http://www.sciencedirect.com/science/article/pii/0005272895000909 ScienceDirect Open Access]
|authors=Kwast KE, Shapiro JI, Rees BB, Hand SC
|authors=Kwast KE, Shapiro JI, Rees BB, Hand SC
|year=1995
|year=1995
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|abstract=The contribution of mitochondrial oxidative phosphorylation to the realkalinization of intracellular pH (pHi) and resynthesis of purine nucleotides during recovery from anoxia was investigated in embryos of Artemia franciscana by assessing the sensitivity of mitochondrial respiration to pH, calculating proton consumption by oxidative phosphorylation, and measuring changes in pHi using 31P nuclear magnetic resonance. Following short-term anoxia, pHi increased from 6.7 to 7.7 during 20 min of aerobic recovery and was temporally correlated with a large increase in ATP. State 3 respiration rates of isolated mitochondria were not substantially compromised at the acidic pH corresponding to the pHiΒ  during anoxia (pH 6.3–6.8) compared to values obtained at pH 7.7. Both state 3 respiration rates and respiratory control ratios exhibited broad, substrate-specific pH optima, whereas state 4 respiration rates increased gradually with increasing pH. P:O flux ratios were near their mechanistic limits and did not vary appreciably with pH below 7.5. Estimates of intracellular buffering capacity indicate that between 18 and 37 mmol H+ (1 cytosol)βˆ’1 must be consumed to elevate pHi from 6.7 to 7.7. Phosphorylation of mono- and diphosphate purine-nucleotides during the first 20 min of recovery may account for the consumption of up to 4.79 mmol H+ (1 cytosol)βˆ’1. An additional 4.77 to 8.18 mmol H+ (1 cytosol)βˆ’1 may be consumed through the oxidation of mono- or dicarboxylic acids, respectively, in the Krebs cycle. Taken together, these data are consistent with a role for oxidative phosphorylation in the realkalinization of pHi and resynthesis of purine nucleotides in A. franciscana embryos during recovery from anoxia.
|abstract=The contribution of mitochondrial oxidative phosphorylation to the realkalinization of intracellular pH (pHi) and resynthesis of purine nucleotides during recovery from anoxia was investigated in embryos of Artemia franciscana by assessing the sensitivity of mitochondrial respiration to pH, calculating proton consumption by oxidative phosphorylation, and measuring changes in pHi using 31P nuclear magnetic resonance. Following short-term anoxia, pHi increased from 6.7 to 7.7 during 20 min of aerobic recovery and was temporally correlated with a large increase in ATP. State 3 respiration rates of isolated mitochondria were not substantially compromised at the acidic pH corresponding to the pHiΒ  during anoxia (pH 6.3–6.8) compared to values obtained at pH 7.7. Both state 3 respiration rates and respiratory control ratios exhibited broad, substrate-specific pH optima, whereas state 4 respiration rates increased gradually with increasing pH. P:O flux ratios were near their mechanistic limits and did not vary appreciably with pH below 7.5. Estimates of intracellular buffering capacity indicate that between 18 and 37 mmol H+ (1 cytosol)βˆ’1 must be consumed to elevate pHi from 6.7 to 7.7. Phosphorylation of mono- and diphosphate purine-nucleotides during the first 20 min of recovery may account for the consumption of up to 4.79 mmol H+ (1 cytosol)βˆ’1. An additional 4.77 to 8.18 mmol H+ (1 cytosol)βˆ’1 may be consumed through the oxidation of mono- or dicarboxylic acids, respectively, in the Krebs cycle. Taken together, these data are consistent with a role for oxidative phosphorylation in the realkalinization of pHi and resynthesis of purine nucleotides in A. franciscana embryos during recovery from anoxia.
|keywords=DatLab - separate application Mitochondrion; Oxidative phosphorylation; pH, intracellular; Respiration; Anoxia; (Artemia)
|keywords=DatLab - separate application Mitochondrion; Oxidative phosphorylation; pH, intracellular; Respiration; Anoxia; (Artemia)
|mipnetlab=US_LA Baton Rouge_Hand SC
|mipnetlab=US_LA Baton Rouge_Hand SC, US IL Urbana Kwast K, US LA New Orleans Rees BB
}}
}}
{{Labeling
{{Labeling

Latest revision as of 09:12, 10 August 2022

Publications in the MiPMap
Kwast KE, Shapiro JI, Rees BB, Hand SC (1995) Oxidative phosphorylation and the realkanization of intracellular pH during recovery from anoxia in Artemia franciscana embryos. Biochim Biophys Acta 1232:5-12.

Β» ScienceDirect Open Access

Kwast KE, Shapiro JI, Rees BB, Hand SC (1995) Biochim Biophys Acta

Abstract: The contribution of mitochondrial oxidative phosphorylation to the realkalinization of intracellular pH (pHi) and resynthesis of purine nucleotides during recovery from anoxia was investigated in embryos of Artemia franciscana by assessing the sensitivity of mitochondrial respiration to pH, calculating proton consumption by oxidative phosphorylation, and measuring changes in pHi using 31P nuclear magnetic resonance. Following short-term anoxia, pHi increased from 6.7 to 7.7 during 20 min of aerobic recovery and was temporally correlated with a large increase in ATP. State 3 respiration rates of isolated mitochondria were not substantially compromised at the acidic pH corresponding to the pHi during anoxia (pH 6.3–6.8) compared to values obtained at pH 7.7. Both state 3 respiration rates and respiratory control ratios exhibited broad, substrate-specific pH optima, whereas state 4 respiration rates increased gradually with increasing pH. P:O flux ratios were near their mechanistic limits and did not vary appreciably with pH below 7.5. Estimates of intracellular buffering capacity indicate that between 18 and 37 mmol H+ (1 cytosol)βˆ’1 must be consumed to elevate pHi from 6.7 to 7.7. Phosphorylation of mono- and diphosphate purine-nucleotides during the first 20 min of recovery may account for the consumption of up to 4.79 mmol H+ (1 cytosol)βˆ’1. An additional 4.77 to 8.18 mmol H+ (1 cytosol)βˆ’1 may be consumed through the oxidation of mono- or dicarboxylic acids, respectively, in the Krebs cycle. Taken together, these data are consistent with a role for oxidative phosphorylation in the realkalinization of pHi and resynthesis of purine nucleotides in A. franciscana embryos during recovery from anoxia. β€’ Keywords: DatLab - separate application Mitochondrion; Oxidative phosphorylation; pH, intracellular; Respiration; Anoxia; (Artemia)

β€’ O2k-Network Lab: US_LA Baton Rouge_Hand SC, US IL Urbana Kwast K, US LA New Orleans Rees BB


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