Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line.
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 (deltapsi(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 cytotoxicity of GD is mainly due to ROS accumulation and ATP depletion in PC12 cells.
Liu
Yan
Y
Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai, China.
Song
Xiao-Dong
XD
Liu
Wen
W
Zhang
Tian-Yi
TY
Zuo
Ji
J
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D016923:Cell Death; D002470:Cell Survival; D005947:Glucose / Q000172:deficiency*; D008564:Membrane Potentials / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress; D016716:PC12 Cells; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D005947:Glucose