PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26223765-10 2015 Lactate decreased pH(i) and nulling the decrease in pH(i) abolished its effects. Lactic Acid 0-7 glucose-6-phosphate isomerase Rattus norvegicus 18-23 26223765-10 2015 Lactate decreased pH(i) and nulling the decrease in pH(i) abolished its effects. Lactic Acid 0-7 glucose-6-phosphate isomerase Rattus norvegicus 52-57 18463242-6 2008 Nonetheless, pHi fell significantly in both cell types when they were treated with exogenous lactate, although 100 microM 4-CIN significantly reduced the magnitude of the acidosis in neurons but not astrocytes. Lactic Acid 93-100 glucose-6-phosphate isomerase Rattus norvegicus 13-16 15261109-9 2004 The results indicate that the anoxic pH(i) decrease is due to enhanced glycolysis and lactate formation with often no obvious effect on K(ATP) channel activity. Lactic Acid 86-93 glucose-6-phosphate isomerase Rattus norvegicus 37-42 11535120-1 2001 When isolated livers from starved rats are perfused with lactate at constant perfusate pH and P(co(2)), there is a marked gradient of cell pH (pH(i)) along the length of the lobular radius, with periportal cells being substantially more alkaline than perivenous cells. Lactic Acid 57-64 glucose-6-phosphate isomerase Rattus norvegicus 143-148 11535120-5 2001 When lactate was removed from the perfusate, mean pH(i) decreased to 7.25. Lactic Acid 5-12 glucose-6-phosphate isomerase Rattus norvegicus 50-55 11535120-7 2001 When lactate was re-introduced mean pH(i) rose to 7.34. Lactic Acid 5-12 glucose-6-phosphate isomerase Rattus norvegicus 36-41 10082802-2 1999 The initial rate of decrease in intracellular pH (pHi) upon lactate or pyruvate incubation was used to determine total transport (carrier mediated and diffusion). Lactic Acid 60-67 glucose-6-phosphate isomerase Rattus norvegicus 50-53 9237533-11 1997 The pH(i) acid shift produced by the increased lactate may contribute to proton modulation of the NMDA receptor and NMDA-induced cell injury or death. Lactic Acid 47-54 glucose-6-phosphate isomerase Rattus norvegicus 4-9 9089688-1 1997 The relationship between glial lactate release and glial intracellular pH (pHi) regulation is studied using C6 glioma cells and rat astrocytes in vitro, and the lactate transport inhibitors quercetin and alpha-cyano-4-hydroxycinnamate (CHC). Lactic Acid 31-38 glucose-6-phosphate isomerase Rattus norvegicus 75-78 9089688-5 1997 A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested by the observation that pHi-homeostasis after acidification by diffusion of undissociated lactic acid into the cell is inhibited by quercetin. Lactic Acid 41-48 glucose-6-phosphate isomerase Rattus norvegicus 68-71 9089688-5 1997 A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested by the observation that pHi-homeostasis after acidification by diffusion of undissociated lactic acid into the cell is inhibited by quercetin. Lactic Acid 41-48 glucose-6-phosphate isomerase Rattus norvegicus 120-123 9089688-5 1997 A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested by the observation that pHi-homeostasis after acidification by diffusion of undissociated lactic acid into the cell is inhibited by quercetin. Lactic Acid 186-197 glucose-6-phosphate isomerase Rattus norvegicus 68-71 9089688-5 1997 A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested by the observation that pHi-homeostasis after acidification by diffusion of undissociated lactic acid into the cell is inhibited by quercetin. Lactic Acid 186-197 glucose-6-phosphate isomerase Rattus norvegicus 120-123 7556881-3 1995 The addition of 20 mM lactate caused a gradual decline in pHi which reversed upon withdrawal of lactate. Lactic Acid 22-29 glucose-6-phosphate isomerase Rattus norvegicus 58-61 7556881-3 1995 The addition of 20 mM lactate caused a gradual decline in pHi which reversed upon withdrawal of lactate. Lactic Acid 96-103 glucose-6-phosphate isomerase Rattus norvegicus 58-61 7859941-8 1995 The early rise in pHi was reduced by external lactate and inhibited by alpha-cyano-4-hydroxycinnamate. Lactic Acid 46-53 glucose-6-phosphate isomerase Rattus norvegicus 18-21 7977806-0 1994 Kinetics of the sarcolemmal lactate carrier in single heart cells using BCECF to measure pHi. Lactic Acid 28-35 glucose-6-phosphate isomerase Rattus norvegicus 89-92 7977806-2 1994 Addition of lactate externally caused a rapid fall of intracellular pH (pHi), which was largely inhibited by 5 mM alpha-cyano-4-hydroxycinnamate (CHC), a specific inhibitor of the lactate carrier. Lactic Acid 12-19 glucose-6-phosphate isomerase Rattus norvegicus 72-75 7977806-2 1994 Addition of lactate externally caused a rapid fall of intracellular pH (pHi), which was largely inhibited by 5 mM alpha-cyano-4-hydroxycinnamate (CHC), a specific inhibitor of the lactate carrier. Lactic Acid 180-187 glucose-6-phosphate isomerase Rattus norvegicus 72-75 7977806-8 1994 Kinetics of lactate efflux were also evaluated using the rate of pHi recovery on removing external lactate. Lactic Acid 12-19 glucose-6-phosphate isomerase Rattus norvegicus 65-68 7977806-8 1994 Kinetics of lactate efflux were also evaluated using the rate of pHi recovery on removing external lactate. Lactic Acid 99-106 glucose-6-phosphate isomerase Rattus norvegicus 65-68 8229818-6 1993 Exposure to 20 mM lactate at the normal extracellular pH (pHo 7.4) for 10 min caused the pHi to fall rapidly by 0.24 pH units and cell shortening was reduced. Lactic Acid 18-25 glucose-6-phosphate isomerase Rattus norvegicus 89-92 8229818-10 1993 During maintained exposure to lactate the pHi remained constant and cell shortening did not recover. Lactic Acid 30-37 glucose-6-phosphate isomerase Rattus norvegicus 42-45 8229818-12 1993 Application of Na(+)-H+ exchanger inhibitors, amiloride or ethylisopropyl-amiloride (EIPA), abolished the recovery of pHi and shortening during maintained exposure to lactate at pHo 7.4 and caused an additional acidosis during maintained application of lactate at pHo 6.4. Lactic Acid 167-174 glucose-6-phosphate isomerase Rattus norvegicus 118-121 8229818-12 1993 Application of Na(+)-H+ exchanger inhibitors, amiloride or ethylisopropyl-amiloride (EIPA), abolished the recovery of pHi and shortening during maintained exposure to lactate at pHo 7.4 and caused an additional acidosis during maintained application of lactate at pHo 6.4. Lactic Acid 253-260 glucose-6-phosphate isomerase Rattus norvegicus 118-121 8229818-20 1993 In conclusion, the Na(+)-H+ exchanger is an important regulator of pHi during a lactate-induced intracellular acidosis. Lactic Acid 80-87 glucose-6-phosphate isomerase Rattus norvegicus 67-70 1417791-2 1992 Glyceraldehyde, lactate and dihydroxyacetone decreased pHi, but only the first two released insulin. Lactic Acid 16-23 glucose-6-phosphate isomerase Rattus norvegicus 55-58 12106379-1 1992 The objective of the present study was to assess the relationship between the amount of lactate accumulated during complete ischaemia and the ensuing changes in extra- and intracellular pH (pHe and pHi, respectively). Lactic Acid 88-95 glucose-6-phosphate isomerase Rattus norvegicus 198-201 12106379-8 1992 The pHi changed from a normal value of approximately 7.0 to 6.5, 6.1 and 5.8 at tissue lactate contents of 10, 20 and 30 mmol kg-1. Lactic Acid 87-94 glucose-6-phosphate isomerase Rattus norvegicus 4-7 2013114-5 1991 For full exploitation of the proton-mediated increase in the cytotoxicity of alkylating agents, pHi should therefore be equilibrated with pHe in lactic acid-producing cells. Lactic Acid 145-156 glucose-6-phosphate isomerase Rattus norvegicus 96-99 2512912-9 1989 It is suggested that this protection of hepatic pHi in DKA may be responsible for the failure of acidotic inhibition of gluconeogenesis from lactate. Lactic Acid 141-148 glucose-6-phosphate isomerase Rattus norvegicus 48-51 3972923-17 1985 It is concluded that the rapid normalization of pHi and overt alkalosis were caused by the simultaneously occurring oxidation of lactate, with the removal of a stoichiometrical amount of H+, and the extrusion of H+ from cells, possibly via a Na+/H+ exchanger, the latter probably delaying normalization of pHe. Lactic Acid 129-136 glucose-6-phosphate isomerase Rattus norvegicus 48-51 6800006-1 1981 The effect of CO2 and of lactic acid (L.A.) on the extracellular (pHe) and intracellular pH (pHi) of ascites tumor cells (DS-carcinosarcoma) in rats was studied by in vitro equilibration of ascites with CO2 and alteration of lactic acid concentration. Lactic Acid 25-36 glucose-6-phosphate isomerase Rattus norvegicus 93-96 6800006-4 1981 pHi exceeded pHe if either PCO2 and/or the concentration of lactic acid was raised above a critical level. Lactic Acid 60-71 glucose-6-phosphate isomerase Rattus norvegicus 0-3 28198-6 1978 In general there were significant positive correlations between intracellular pH (pHi) and hepatocyte phosphoenolpyruvate, 2-phosphoglycerate and 3-phosphoglycerate concentrations, and negative correlations between pHi and lactate and pyruvate concentrations; there were usually significant correlations in the opposite sense between these metabolites and log PCO2. Lactic Acid 223-230 glucose-6-phosphate isomerase Rattus norvegicus 82-85 34052758-7 2021 Activating AMPK inhibited the production of lactate and pyruvate by suppressing the expression of glycolysis-related genes HK1, Pgam1, and Gpi1 and that of lactate production-related proteins LDHA and MCT4. Lactic Acid 44-51 glucose-6-phosphate isomerase Rattus norvegicus 139-143