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Free Radic Biol Med

Title:		Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells
Author(s):		Chen SJ; Wang JL; Chen JH; Huang RN;
Address:		"Department of Botany, National Taiwan University, Taipei, Taiwan, Republic of China"
Journal Title:		Free Radic Biol Med
Year:		2002
Volume:		33
Issue:		4
Page Number:		464 - 472
DOI:		10.1016/s0891-5849(02)00817-1
ISSN/ISBN:		0891-5849 (Print) 0891-5849 (Linking)
Abstract:		"Trichloroethylene (TCE) and perchloroethylene (PERC) are volatile organic compounds (VOCs) that are primarily inhaled through the respiratory system. The aim of this study was to elucidate the role of glutathione (GSH) and p53 in TCE- and PERC-induced lung toxicity. Human lung adenocarcinoma cells NCI-H460 (p53-wild-type) have constitutively lower levels of GSH than NCI-H1299 (p53-null) cells. The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells. The accumulation of H(2)O(2) was accompanied by severe cellular damage, as indicated by the significant increase of lipid peroxidation and apoptosis in p53-WT H460 cells, but not p53-null H1299 cells. Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation. In contrast, depletion of GSH in p53-null H1299 cells enhanced TCE- or PERC-induced lipid peroxidation. The levels of p53 and Bax proteins were elevated, while Bcl-2 protein was downregulated in TCE- or PERC-treated p53-WT H460 cells. Activity of caspase 3, the apoptotic executioner, was also significantly enhanced in TCE- or PERC-treated cells. These data suggest that, in human lung cancer cells, GSH plays a vital role in the protection of TCE- and PERC-induced oxidative stress and apoptosis, which may be mediated through a p53-dependent pathway"
Keywords:		"Adenocarcinoma/metabolism/*pathology Apoptosis/*drug effects/physiology Caspase 3 Caspases/metabolism Enzyme Activation/drug effects Free Radical Scavengers/pharmacology Gases Gene Expression Regulation, Neoplastic/drug effects Glutathione/*physiology Hum;"
Notes:		"MedlineChen, Shiang-Jiuun Wang, Jia-Lin Chen, Jian-Hung Huang, Rong-Nan eng Comparative Study Research Support, Non-U.S. Gov't 2002/08/06 Free Radic Biol Med. 2002 Aug 15; 33(4):464-72. doi: 10.1016/s0891-5849(02)00817-1"