Premium
2,4‐Dinitrophenol induces apoptosis in As4.1 juxtaglomerular cells through rapid depletion of GSH
Author(s) -
Han Yong Hwan,
Kim Sung Zoo,
Kim Suhn Hee,
Park Woo Hyun
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.08.023
Subject(s) - intracellular , apoptosis , annexin , tiron , 2,4 dinitrophenol , reactive oxygen species , catalase , glutathione , microbiology and biotechnology , chemistry , programmed cell death , mitochondrion , dinitrophenol , biochemistry , biology , oxidative stress , superoxide , enzyme
2,4‐Dinitrophenol (DNP) is an uncoupler of oxidative phosphorylation in mitochondria. Here, we investigated the in vitro effect of DNP on apoptosis and the involvement of reactive oxygen species (ROS) in As4.1 juxtaglomerular cell death. Dose‐ and time‐dependent induction of apoptosis was evidenced by flow cytometric detection of sub‐G1 DNA content and annexin V binding assay. The intracellular H 2 O 2 and O 2 − levels were markedly increased in DNP‐treated cells. However, the reduction of intracellular H 2 O 2 level by Tiron and catalase did not prevent apoptosis induced by DNP. Moreover, DNP rapidly reduced intracellular GSH content in As4.1 cells. Taken together, apoptosis in DNP‐treated As4.1 cells is correlated with the rapid change of intracellular GSH levels rather than ROS levels.