4.7 Article

Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells

Journal

APOPTOSIS
Volume 14, Issue 2, Pages 218-225

Publisher

SPRINGER
DOI: 10.1007/s10495-008-0295-5

Keywords

Sodium selenite; Apoptosis; ER stress; GADD153; ROS

Funding

  1. National Natural Sciences Foundation of China [30370348, 30770491]
  2. Doctoral Point Foundation of National Educational Committee [20010023029]
  3. Natural Sciences Foundation of Beijing [7032034, 5082015]

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In this study, we delineated the apoptotic signaling pathways activated by sodium selenite in NB4 cells. NB4 cells were treated with 20 mu M sodium selenite for different times. The activation of caspases and ER stress markers, ROS levels, mitochondrial membrane potential and cell apoptosis induced by sodium selenite were analyzed by immunoblotting analysis, DCF fluorescence and flow cytometric respectively. siRNA was used to detect the effect of GADD153 on selenite-induced cell apoptosis. Sodium selenite-induced reactive oxygen species generation is an early event that triggers endoplasmic reticulum stress mitochondrial apoptotic pathways in NB4 cells.

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