Mechanism of the apoptosis of rat pancreas islet β cell strain (INS-1 cells) induced by sodium arsenite.
- Author:
Xiao PAN
1
;
Li-ping JIANG
;
Lai-fu ZHONG
;
Cheng-yan GENG
;
Xian-ce SUN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Arsenites; toxicity; Cells, Cultured; Insulin-Secreting Cells; drug effects; Lysosomes; metabolism; Membrane Potentials; drug effects; Mitochondria; metabolism; Rats; Sodium Compounds; toxicity
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2012;30(7):481-484
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study mechanism of the apoptosis of rat pancreas islet β cell strain (INS-1 cells) induced by sodium arsenite.
METHODSINS-1 cells were exposed to sodium arsenite at the different concentrations. MTT assay was used to detect the viability of INS-1 cells. The potentials on mitochondrial membrane and lysosome membrane of INS-1 cells were determined with the fluorescence spectrophotometer. The apoptotic levels of INS-1 cells exposed to sodium arsenite were observed by a fluorescence microscope and flow cytometry.
RESULTSAfter exposure to sodium arsenite, the viability of INS-1 cells significantly decreased with the doses of sodium arsenite. At 24 h after exposure, the OD values of the mitochondrial membrane potentials declined observably with the doses of sodium arsenite (P < 0.01). At 48 h after exposure, the OD values of the lysosome membrane potentials significantly increased with the doses of sodium arsenite (P < 0.01). At 72 h after exposure, the apoptotic cells were observed under a fluorescence microscope and enhanced with the doses of sodium arsenite. The apoptosis cells with light blue, karyopyknosis, karyorrhexis, apoptotic body and chromatin concentration appeared. The results detected with flow cytometry indicated that after exposure, the apoptotic INS-1E cells significantly increased with the doses of sodium arsenite.
CONCLUSIONSThe sodium arsenite can induce the apoptosis of INS-1 cells through the mitochondria-lysosome pathway.