title: Apoptosis in pyrogallol-treated Calu-6 cells is correlated with the changes of intracellular GSH levels rather than ROS levels.
abstract: We investigated the involvement of glutathione (GSH) and reactive oxygen species (ROS) such as H2O2 and O2-* in the deaths of pyrogallol-treated Calu-6 cells. Pyrogallol inhibited the growth of Calu-6 cells with an IC50 of approximately 50 microM. Levels of intracellular H2O2 were not altered or were decreased in pyrogallol-treated Calu-6 cells at 72 h. However, levels of O2*- were increased. Treatment with pyrogallol also reduced the intracellular GSH content. The activity of SOD was down-regulated, but the activity of catalase was up-regulated by pyrogallol at 72 h. ROS scavengers, including Tempol, Tiron, Trimetazidine, and N-acetylcysteine (NAC), did not reduce the levels of the intracellular O2*-. Tempol showing the recovery of GSH depletion in pyrogallol-treated cells significantly prevented apoptosis, while Tiron prevented the loss of mitochondrial transmembrane potential (DeltaPsi(m)). In contrast, treatment with NAC showing an increased effect on O2*- levels and depletion of GSH intensified pyrogallol-induced apoptosis. In addition, treatment with SOD and catalase significantly prevented the loss of mitochondrial transmembrane potential (DeltaPsi(m)) in pyrogallol-treated Calu-6 cells. However, only catalase showing a decreased effect on O2*- levels and depletion of GSH prevented pyrogallol-induced apoptosis. Taken together, apoptosis in pyrogallol-treated Calu-6 cells is correlated with the changes of intracellular GSH levels rather than ROS levels.
authors.affiliation: Department of Physiology, Medical School, Research Institute of Clinical Medicine, Centers for Healthcare Technology Development, Chonbuk National University, JeonJu 561-180, Republic of Korea.
authors.forename: Yong Hwan
authors.initials: YH
authors.lastname: Han
authors.forename: Sung Zoo
authors.initials: SZ
authors.lastname: Kim
authors.forename: Suhn Hee
authors.initials: SH
authors.lastname: Kim
authors.forename: Woo Hyun
authors.initials: WH
authors.lastname: Park
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism*; D000704:Analysis of Variance; D000975:Antioxidants / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D002374:Catalase / Q000378:metabolism; D003497:Cyclic N-Oxides; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism*; D008564:Membrane Potentials; D011748:Pyrogallol / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013113:Spin Labels; D013482:Superoxide Dismutase / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000975:Antioxidants; D003497:Cyclic N-Oxides; D017382:Reactive Oxygen Species; D013113:Spin Labels; D011748:Pyrogallol; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; C001803:tempol