pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells
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pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells. / Litman, Thomas; Pedersen, S F; Kramhøft, B; Skovsgaard, T; Hoffmann, E K.
In: Cellular Physiology and Biochemistry, Vol. 8, No. 3, 1998, p. 138-50.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells
AU - Litman, Thomas
AU - Pedersen, S F
AU - Kramhøft, B
AU - Skovsgaard, T
AU - Hoffmann, E K
PY - 1998
Y1 - 1998
N2 - Maintenance and regulation of intracellular pH (pHi) was studied in wild-type Ehrlich ascites tumor cells (EHR2) and five progressively daunorubicin-resistant, P-glycoprotein (P-gp)-expressing strains, the maximally resistant of which is EHR2/1.3. Steady-state pHi was similar in cells expressing different amounts of P-gp, in the absence and presence of glucose. In EHR2/1.3, glucose-induced acidification was reduced, and proton efflux was increased, compared to the wild-type EHR2, differences which were not caused by increased activity of a Na+/H+ exchanger in the resistant cells. Comparing all six cell lines, no evidence was found for a correlation between the amount of P-gp in the membrane and pHi regulation, which was also unaffected by P-gp modulators. However, a correlation was seen between relative resistance/daunorubicin accumulation and acid extrusion rate, which is likely to be due to aspects of development of drug resistance other than P-gp.
AB - Maintenance and regulation of intracellular pH (pHi) was studied in wild-type Ehrlich ascites tumor cells (EHR2) and five progressively daunorubicin-resistant, P-glycoprotein (P-gp)-expressing strains, the maximally resistant of which is EHR2/1.3. Steady-state pHi was similar in cells expressing different amounts of P-gp, in the absence and presence of glucose. In EHR2/1.3, glucose-induced acidification was reduced, and proton efflux was increased, compared to the wild-type EHR2, differences which were not caused by increased activity of a Na+/H+ exchanger in the resistant cells. Comparing all six cell lines, no evidence was found for a correlation between the amount of P-gp in the membrane and pHi regulation, which was also unaffected by P-gp modulators. However, a correlation was seen between relative resistance/daunorubicin accumulation and acid extrusion rate, which is likely to be due to aspects of development of drug resistance other than P-gp.
KW - Amiloride
KW - Animals
KW - Buffers
KW - Carcinoma, Ehrlich Tumor
KW - Drug Resistance, Multiple
KW - Drug Resistance, Neoplasm
KW - Glucose
KW - Hydrogen-Ion Concentration
KW - Ion Transport
KW - P-Glycoprotein
KW - Protons
KW - Tumor Cells, Cultured
M3 - Journal article
C2 - 9617476
VL - 8
SP - 138
EP - 150
JO - Cellular Physiology and Biochemistry
JF - Cellular Physiology and Biochemistry
SN - 1015-8987
IS - 3
ER -
ID: 119647665