Premium
Docosahexaenoic acid and other fatty acids induce a decrease in pH i in Jurkat T‐cells
Author(s) -
Aires Virginie,
Hichami Aziz,
Moutairou Kabirou,
Khan Naim Akhtar
Publication year - 2003
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705563
Subject(s) - docosahexaenoic acid , bapta , intracellular ph , eicosapentaenoic acid , arachidonic acid , chemistry , calcium , biochemistry , fatty acid , amiloride , dids , sodium calcium exchanger , biophysics , intracellular , polyunsaturated fatty acid , biology , sodium , membrane , organic chemistry , enzyme
Docosahexaenoic acid (DHA) induced rapid ( t 1/2 =33 s) and dose‐dependent decreases in pH i in BCECF‐loaded human (Jurkat) T‐cells. Addition of 5‐( N , N ‐dimethyl)‐amiloride, an inhibitor of Na + /H + exchanger, prolonged DHA‐induced acidification as a function of time, indicating that the exchanger is implicated in pH i recovery. Other fatty acids like oleic acid, arachidonic acid, eicosapentaenoic acid, but not palmitic acid, also induced a fall in pH i in these cells. To assess the role of calcium in the DHA‐induced acidification, we conducted experiments in Ca 2+ ‐free (0% Ca 2+ ) and Ca 2+ ‐containing (100% Ca 2+ ) buffer. We observed that there was no difference in the degree of DHA‐induced transient acidification in both the experimental conditions, though pH i recovery was faster in 0% Ca 2+ medium than that in 100% Ca 2+ medium. In the presence of BAPTA, a calcium chelator, a rapid recovery of DHA‐induced acidosis was observed. Furthermore, addition of CaCl 2 into 0% Ca 2+ medium curtailed DHA‐evoked rapid pH i recovery. In 0% Ca 2+ medium, containing BAPTA, DHA did not evoke increases in [Ca 2+ ] i , though this fatty acid still induced a rapid acidification in these cells. These observations suggest that calcium is implicated in the long‐lasting DHA‐induced acidosis. DHA‐induced rapid acidification may be due to its deprotonation in the plasma membrane (flip‐flop model), as suggested by the following observations: (1) DHA with a –COOH group induced intracellular acidification, but this fatty acid with a –COOCH 3 group failed to do so, and (2) DHA, but not propionic acid, ‐induced acidification was completely reversed by addition of fatty acid‐free bovine serum albumin in these cells. These results suggest that DHA induces acidosis via deprotonation and Ca 2+ mobilization in human T‐cells.British Journal of Pharmacology (2003) 140 , 1217–1226. doi: 10.1038/sj.bjp.0705563