pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

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

Harvard

Litman, T, Pedersen, SF, Kramhøft, B, Skovsgaard, T & Hoffmann, EK 1998, 'pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells', Cellular Physiology and Biochemistry, vol. 8, no. 3, pp. 138-50.

APA

Litman, T., Pedersen, S. F., Kramhøft, B., Skovsgaard, T., & Hoffmann, E. K. (1998). pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells. Cellular Physiology and Biochemistry, 8(3), 138-50.

Vancouver

Litman T, Pedersen SF, Kramhøft B, Skovsgaard T, Hoffmann EK. pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells. Cellular Physiology and Biochemistry. 1998;8(3):138-50.

Author

Litman, Thomas ; Pedersen, S F ; Kramhøft, B ; Skovsgaard, T ; Hoffmann, E K. / pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells. In: Cellular Physiology and Biochemistry. 1998 ; Vol. 8, No. 3. pp. 138-50.

Bibtex

@article{ae631589e5894b74bc0c729467eb1d97,
title = "pH regulation in sensitive and multidrug resistant Ehrlich ascites tumor cells",
abstract = "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.",
keywords = "Amiloride, Animals, Buffers, Carcinoma, Ehrlich Tumor, Drug Resistance, Multiple, Drug Resistance, Neoplasm, Glucose, Hydrogen-Ion Concentration, Ion Transport, P-Glycoprotein, Protons, Tumor Cells, Cultured",
author = "Thomas Litman and Pedersen, {S F} and B Kramh{\o}ft and T Skovsgaard and Hoffmann, {E K}",
year = "1998",
language = "English",
volume = "8",
pages = "138--50",
journal = "Cellular Physiology and Biochemistry",
issn = "1015-8987",
publisher = "S Karger AG",
number = "3",

}

RIS

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