Diesel Exhaust Particle-Induced Cell Death of Cultured Normal Human Bronchial Epithelial Cells

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概要

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• We investigated the effect of diesel exhaust particles (DEPs) on normal human bronchial epithelial (NHBE) cells. Inclusion of DEPs in culture media was lethal to NHBE cells. NHBE cells are more susceptible to DEPs than other normal human lung cells, normal human pulmonary artery endothelial cells and normal human embryonic lung fibroblasts. DEP-induced cell death was mainly due to necrosis. Using the fluorescence probes diacetoxymethyl 6-carboxy-3',6'-diacetoxy-2',7'-dichloro-3',6'-dideoxydihydrofluorescinate and 4.5-diaminofluo rescein diacetate, it was observed that hydrogen peroxide and nitrogen monoxide, respectively, were generated within DEP-exposed NHBE cells. DEP cytotoxicity increased or decreased with an increase or decrease in the cellular level of reduced glutathione (GSH) by treatment with L-buthioninc-(R,S)-sulfoximine or ethyl reduced glutathionate, respectively. In addition, DEPs themselves decreased the cellular level of GSH in a dose-dependent manner. Upon exposure of NHBE cells to high concentrations of DEPs, their cellular GSH was depleted almost throughout. Further, the following agents decreased DEP cytotoxicity: 1) antioxidants 2,2,5,7,8-pentamethylchro man-6'o1, ebselen, and N,NV'-bis(salicylidene)etnylenediaminomanganese(II) dihydrate (EUK-8); 2) iron ionchelating agents disodium bathophenanthrolinedisulfonate and desferrioxamine mesylate; 3) nitrogen monoxide synthase inhibitors N^G-nitro-L-arginine methyl ester hydrochloride and N^G-methyl-L-arginine acetate salt; and 4) an endocytosis inhibitor quinacrine. On the basis of these observations, the mechanism of DEP cytotoxicity toward IVHBE cells is discussed.

• 公益社団法人日本薬学会の論文
• 2003-04-01

著者

• Sagai Masaru

  Division Of Nursing And Human Sciences Faculty Of Health Sciences Aomori University Of Health And We

• Shimada Toshio

  Department of Cardiology, Shimane University School of Medicine

• Shimada T

  Department Of Biology Faculty Of Science And High Technology Research Center Konan University

• Suzuki Motohisa

  Graduate School Of Health Sciences University Of Shizuoka

• Sasaki N

  Department Of Biology Faculty Of Science And High Technology Research Center Konan University

• Sasaki Naoko

  Department Of Biology Faculty Of Science And High Technology Research Center Konan University

• MATSUO Mitsuyoshi

  Department of Biology, Faculty of Science and High Technology Research Center, Konan University

• Uenishi Rie

  Department Of Biology Faculty Of Science And High Technology Research Center Konan University

• Matsuo Mitsuyoshi

  Department Of Biology Faculty Of Science And High Technology Research Center Konan University

• Sagai Masaru

  Division Of Human Sciences Faculty Of Health Sciences Aomori University Of Health And Welfare

• Shimada Toshio

  Department of Biology, Faculty of Science and High Technology Research Center, Konan University

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