These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: The influence of an uncoupler on amino acid accumulation in Ehrlich mouse ascites tumor cells.
    Author: Burckhardt G, Pietrzyk C.
    Journal: Biochim Biophys Acta; 1980 Sep 18; 601(2):403-14. PubMed ID: 7407176.
    Abstract:
    In Ehrlich ascites tumor cells, carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) acts at two different sites depending upon the concentration employed. (1) In non-glycolysing respiring cells, FCCP is seen to uncouple the mitochondria and thereby it inhibits the ATP-dependent (Na+, K+) pump. (2) In glycolysing cells, FCCP does not affect the electrogenic (Na+, K+) pump, but depolarizes the plasma membrane potential difference as visualized by the distribution of the lipid-soluble cation, tetraphenylphosphonium, and by an inhibition of the rheogenic, Na+-dependent uptake of alpha-aminoisobutyric acid. A depolarization by FCCP also occurs under conditions where a K+-diffusion potential is present and the pump is blocked by metabolic inhibition or by ouabain. Depolarization and FCCP-induced increase in H+ fluxes across the plasma membrane exhibit a similar FCCP-concentration dependency. The imposition of proton-concentration differences in the presence of FCCP inhibits (pHi > pHo) or stimulates (pHi < pHo) alpha-aminoisobutyric acid uptake and tetraphenylphosphonium accumulation. The experiments indicate that FCCP shifts the plasma membrane potential of Ehrlich cells, which are normally relatively impermeable for protons, towards an H+-diffusion potential.
    [Abstract] [Full Text] [Related] [New Search]