Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | American Journal of Physiology: Cell Physiology |
| Vol/bind | 293 |
| Udgave nummer | 1 |
| Sider (fra-til) | C390-400 |
| ISSN | 0363-6143 |
| DOI | |
| Status | Udgivet - 2007 |
Bibliografisk note
Keywords: Animals; Antioxidants; Arachidonate 5-Lipoxygenase; Arachidonic Acid; Carcinoma, Ehrlich Tumor; Cell Line, Tumor; Cell Size; Dose-Response Relationship, Drug; Enzyme Inhibitors; Fibroblasts; Hydrogen Peroxide; Hypotonic Solutions; Lipoxygenase Inhibitors; Mice; NADPH Oxidase; NIH 3T3 Cells; Naphthalenes; Onium Compounds; Phospholipases A; Protein Tyrosine Phosphatases; Pyrones; Reactive Oxygen Species; Signal Transduction; Sodium Chloride; Taurine; Terpenes; Time Factors; VanadatesAdgang til dokumentet
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I: American Journal of Physiology: Cell Physiology, Bind 293, Nr. 1, 2007, s. C390-400.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Activation and inactivation of the volume-sensitive taurine leak pathway in NIH3T3 fibroblasts and Ehrlich Lettre ascites cells.
AU - Lambert, Ian Henry
N1 - Keywords: Animals; Antioxidants; Arachidonate 5-Lipoxygenase; Arachidonic Acid; Carcinoma, Ehrlich Tumor; Cell Line, Tumor; Cell Size; Dose-Response Relationship, Drug; Enzyme Inhibitors; Fibroblasts; Hydrogen Peroxide; Hypotonic Solutions; Lipoxygenase Inhibitors; Mice; NADPH Oxidase; NIH 3T3 Cells; Naphthalenes; Onium Compounds; Phospholipases A; Protein Tyrosine Phosphatases; Pyrones; Reactive Oxygen Species; Signal Transduction; Sodium Chloride; Taurine; Terpenes; Time Factors; Vanadates
PY - 2007
Y1 - 2007
N2 - Hypotonic exposure provokes the mobilization of arachidonic acid, production of ROS, and a transient increase in taurine release in Ehrlich Lettre cells. The taurine release is potentiated by H(2)O(2) and the tyrosine phosphatase inhibitor vanadate and reduced by the phospholipase A(2) (PLA(2)) inhibitors bromoenol lactone (BEL) and manoalide, the 5-lipoxygenase (5-LO) inhibitor ETH-615139, the NADPH oxidase inhibitor diphenyl iodonium (DPI), and antioxidants. Thus, swelling-induced taurine efflux in Ehrlich Lettre cells involves Ca(2+)-independent (iPLA(2))/secretory PLA(2) (sPLA(2)) plus 5-LO activity and modulation by ROS. Vanadate and H(2)O(2) stimulate arachidonic acid mobilization and vanadate potentiates ROS production in Ehrlich Lettre cells and NIH3T3 fibroblasts under hypotonic conditions. However, vanadate-induced potentiation of the volume-sensitive taurine efflux is, in both cell types, impaired in the presence of BEL and DPI and following restoration of the cell volume. Thus, potentiation of the volume-sensitive taurine efflux pathway following inhibition of tyrosine phosphatase activity reflects increased arachidonic acid mobilization and ROS production for downstream signaling. Vanadate delays the inactivation of volume-sensitive taurine efflux in NIH3T3 cells, and this delay is impaired in the presence of DPI. Vanadate has no effect on the inactivation of swelling-induced taurine efflux in Ehrlich Lettre cells. It is suggested that increased tyrosine phosphorylation of regulatory components of NADPH oxidase leads to increased ROS production and a subsequent delay in inactivation of the volume-sensitive taurine efflux pathway and that NADPH oxidase or antioxidative capacity differ between NIH3T3 and Ehrlich Lettre cells.
AB - Hypotonic exposure provokes the mobilization of arachidonic acid, production of ROS, and a transient increase in taurine release in Ehrlich Lettre cells. The taurine release is potentiated by H(2)O(2) and the tyrosine phosphatase inhibitor vanadate and reduced by the phospholipase A(2) (PLA(2)) inhibitors bromoenol lactone (BEL) and manoalide, the 5-lipoxygenase (5-LO) inhibitor ETH-615139, the NADPH oxidase inhibitor diphenyl iodonium (DPI), and antioxidants. Thus, swelling-induced taurine efflux in Ehrlich Lettre cells involves Ca(2+)-independent (iPLA(2))/secretory PLA(2) (sPLA(2)) plus 5-LO activity and modulation by ROS. Vanadate and H(2)O(2) stimulate arachidonic acid mobilization and vanadate potentiates ROS production in Ehrlich Lettre cells and NIH3T3 fibroblasts under hypotonic conditions. However, vanadate-induced potentiation of the volume-sensitive taurine efflux is, in both cell types, impaired in the presence of BEL and DPI and following restoration of the cell volume. Thus, potentiation of the volume-sensitive taurine efflux pathway following inhibition of tyrosine phosphatase activity reflects increased arachidonic acid mobilization and ROS production for downstream signaling. Vanadate delays the inactivation of volume-sensitive taurine efflux in NIH3T3 cells, and this delay is impaired in the presence of DPI. Vanadate has no effect on the inactivation of swelling-induced taurine efflux in Ehrlich Lettre cells. It is suggested that increased tyrosine phosphorylation of regulatory components of NADPH oxidase leads to increased ROS production and a subsequent delay in inactivation of the volume-sensitive taurine efflux pathway and that NADPH oxidase or antioxidative capacity differ between NIH3T3 and Ehrlich Lettre cells.
U2 - 10.1152/ajpcell.00104.2007
DO - 10.1152/ajpcell.00104.2007
M3 - Journal article
C2 - 17537804
SN - 0363-6143
VL - 293
SP - C390-400
JO - American Journal of Physiology: Cell Physiology
JF - American Journal of Physiology: Cell Physiology
IS - 1
ER -