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Related Experiment Videos

Docosahexaenoic acid and other fatty acids induce a decrease in pHi in Jurkat T-cells.

Virginie Aires1, Aziz Hichami, Kabirou Moutairou

  • 1UPRES Lipides and Nutrition, Université de Bourgogne, Faculté des Sciences de la vie, 6, Boulevard Gabriel, Dijon 21000, France.

British Journal of Pharmacology
|December 4, 2003
PubMed
Summary

Docosahexaenoic acid (DHA) rapidly decreases intracellular pH in human T-cells, involving the Na+/H+ exchanger and calcium. This acidification mechanism is linked to DHA deprotonation and calcium mobilization.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Intracellular pH (pHi) regulation is crucial for T-cell function.
  • Docosahexaenoic acid (DHA) is a key omega-3 fatty acid with known biological effects.

Purpose of the Study:

  • To investigate the effect of DHA on intracellular pH in human T-cells.
  • To elucidate the mechanisms underlying DHA-induced intracellular acidification and pHi recovery.

Main Methods:

  • Human Jurkat T-cells loaded with BCECF were used to measure pHi.
  • Experiments involved varying calcium concentrations and using inhibitors like 5-(N,N-dimethyl)-amiloride and BAPTA.
  • Fatty acid modifications and bovine serum albumin were employed to explore the acidification mechanism.

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Main Results:

  • DHA induced rapid, dose-dependent decreases in pHi, with recovery influenced by the Na+/H+ exchanger.
  • Other unsaturated fatty acids also caused pHi fall, but palmitic acid did not.
  • Calcium plays a role in the prolonged DHA-induced acidosis, though not in the initial acidification.
  • Evidence suggests DHA deprotonation in the plasma membrane contributes to acidification.

Conclusions:

  • DHA induces rapid intracellular acidosis in human T-cells via deprotonation.
  • Calcium mobilization is implicated in the sustained phase of DHA-induced acidosis.
  • The Na+/H+ exchanger is involved in restoring normal pHi after DHA exposure.