Open AccessGlucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line
Author(s) -
Liu Yan,
Song XiaoDong,
Liu Wen,
Zhang TianYi,
Zuo Ji
Publication year - 2003
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2003.tb00202.x
Subject(s) - propidium iodide , oxidative stress , reactive oxygen species , mitochondrion , apoptosis , intracellular , mtt assay , viability assay , membrane potential , mitochondrial permeability transition pore , necrosis , chemistry , microbiology and biotechnology , biology , endocrinology , medicine , programmed cell death , biochemistry
Glucose metabolism plays a pivotal role in many physiological and pathological conditions. To investigate the effect of hypoglycemia (obtained by glucose deprivation) on PC12 cell line, we analyzed the cell viability, mitochondrial function (assessed by MTT reduction, cellular ATP level, mitochondrial transmembrane potential), and the level of reactive oxygen species (ROS) after glucose deprivation (GD). Upon exposure to GD, ROS level increased and MTT reduction decreased immediately, intracellular ATP level increased in the first 3 hours, followed by progressive decrease till the end of GD treatment, and the mitochondrial transmembrane potential (ΔΨ m ) dropped after 6 hours. Both necrosis and apoptosis occurred apparently after 24 hours which was determined by nuclei staining with propidium iodide(PI) and Hoechst 33342. These data suggested that cytotoxity of GD is mainly due to ROS accumulation and ATP depletion in PC12 cells.