Curcumin binds tubulin, induces mitotic catastrophe, and impedes normal endothelial cell proliferation

Steven J.T. Jackson, Laura L. Murphy, Richard C. Venema, Keith W. Singletary, Andrew J. Young

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

Curcumin, a component of turmeric spice that imparts flavor and color to curry, is thought to possess anti-inflammatory and antioxidant properties in biological tissues. However, while such efficacies have been described in the context of carcinogenesis, the impact of curcumin on normal cell cycle regulation is poorly understood. Here, we provide evidence of curcumin toxicity in proliferating bovine aortic endothelial cells, at concentrations relevant to the diet and below those previously reported in cancer models. Upon confirming curcumin's ability to upregulate hemeoxygenase-1 in a dose-dependent fashion, we found the minimally efficacious curcumin concentration to also inhibit endothelial cell DNA synthesis. Moreover, curcumin concentrations below the minimum 2. μM threshold required to induce hemeoxygenase-1 bound tubulin protein in vitro and triggered hallmark evidence of mitotic catastrophe in vivo. Concentrations as low as 0.1. μM curcumin led to disproportionate DNA segregation, karyorrhexis, and micronucleation in proliferating endothelial cells. While suggesting a mechanism by which physiological curcumin concentrations inhibit cell cycle progression, these findings describe heretofore unappreciated curcumin toxicity with potential implications for endothelial growth, development, and tissue healing.

Original languageEnglish (US)
Pages (from-to)431-438
Number of pages8
JournalFood and Chemical Toxicology
Volume60
DOIs
StatePublished - Oct 1 2013

Keywords

  • Cell cycle
  • Curcumin
  • Endothelial
  • Tubulin

ASJC Scopus subject areas

  • Food Science
  • Toxicology

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