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Journal of Cellular and Molecular Medicine logoLink to Journal of Cellular and Molecular Medicine
. 2007 May 1;7(1):49–56. doi: 10.1111/j.1582-4934.2003.tb00202.x

Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line

Yan Liu 1,2, Xiao‐Dong Song 1, Wen Liu 1, Tian‐Yi Zhang 2, Ji Zuo 1,
PMCID: PMC6740129  PMID: 12767261

Abstract

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 (ΔΨm) 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.

Keywords: glucose deprivation, ATP depletion, mitochondrial membrane potential, reactive oxygen species, apoptosis, necrosis

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