Apoptosis in human aortic endothelial cells induced by hyperglycemic condition involves mitochondrial depolarization and is prevented by N-acetyl-L-cysteine.

Rina Recchioni, Fiorella Marcheselli, Fausto Moroni, Carlo Pieri

Research output: Contribution to journalArticle

Abstract

We investigated whether the dissipation of mitochondrial transmembrane potential (Delta(Psi)(m)) was involved in apoptosis of cultured human aortic endothelial cells (HAECs) exposed to hyperglycemic conditions (30 mmol/L glucose). In parallel experiments, N-acetyl-L-cysteine (NAC) was added to the culture medium to verify whether this antioxidant may prevent apoptosis in these cells. The binding of annexin V and DNA fragmentation were measured, in addition to the production of reactive oxygen species (ROS), the number of cells with depolarized mitochondria, and the intracellular glutathione (GSH) content. As compared to the control (5 mmol/L glucose), high-glucose treatment increases both ROS generation and the number of cells binding annexin V. Moreover, a simultaneous decrease of intracellular GSH content was observed, which was accompanied by an increased number of cells showing both depolarized mitochondria and fragmented DNA. Incubation of HAECs with high glucose in the presence of 10 mmol/L NAC prevented the drop of intracellular GSH content, and decreased both ROS generation and the number of cells committed to apoptosis. These results suggest that high glucose triggers the same cascade of molecular events as do other apoptosis inducers in other cells. Among these events, the disruption of mitochondrial membrane barrier function might be decisive because it causes the release of soluble proteins from intermembrane space, which then induce nuclear apoptotic changes.

Original languageEnglish
Pages (from-to)1384-1388
Number of pages5
JournalMetabolism
Volume51
Issue number11
Publication statusPublished - Nov 2002

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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