(-)-Epicatechin and related procyanidins modulate intracellular calcium and prevent oxidation in Jurkat T cells

Sandra V. Verstraeten, Gerardo Mackenzie, Patricia I. Oteiza, Cesar G. Fraga

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

This study investigated the effects of (-)-epicatechin (EC), its oligomers, dimer B2 (B2) and trimer C1 (C1), on calcium-dependent cell oxidation. Jurkat T cells were subjected to a Ca2+ mobilization challenge by replacing Na+ with K+ in the incubation media. A 249±38% increase in intracellular Ca2+ concentration ([Ca2+]i) was observed and that effect was prevented by the presence of inhibitors of Ca2+ mobilization and entrance. The pre-incubation of the cells in the presence of EC, B2 or C1 prevented K2+-mediated increase in [Ca2+]i. IC50 were 10, 24 and 196 nm for EC, B2 and C1, respectively. Cell membrane depolarization was affected by K2+, but neither inhibitors of Ca2+ mobilization nor EC, B2 or C1 modified the increase in membrane potential. An 84±7% increase in cell oxidants was observed after cell exposure to K+. This increase was prevented by the inhibition of Ca2+ mobilization, NADPH oxidase and protein kinase C, as well as by 10 nm EC, 10 nm B2 or 100 nm C1. In addition, EC and B2 (100 nm) significantly inhibited the activation of the [Ca2+]i-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca2+] i and then prevent cell oxidation and other Ca2+ -regulated events.

Original languageEnglish (US)
Pages (from-to)864-872
Number of pages9
JournalFree Radical Research
Volume42
Issue number10
DOIs
StatePublished - 2008

Keywords

  • Antioxidant
  • Calcium channels
  • Cocoa
  • Flavanol
  • Flavonoid
  • Gastrointestinal tract
  • Inflammation
  • Membrane interactions
  • Oxidation
  • Procyanidin

ASJC Scopus subject areas

  • Biochemistry

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