Protein carbonylation in THP-1 cells induced by cigarette smoke extract via a copper-catalyzed pathway

doi:10.1021/tx900008h

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 生物醫學科學學系暨碩士班 > 期刊論文 > Item 310902500/18055

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18055

Title:	Protein carbonylation in THP-1 cells induced by cigarette smoke extract via a copper-catalyzed pathway
Authors:	Lin, C.-C.;Su, T.-H.;Wang, T.-S.
Date:	2009
Issue Date:	2017-08-01T08:17:49Z (UTC)
ISSN:	0893228X
Abstract:	Cigarette smoke is a mixture of chemicals that cause direct or indirect oxidative stress in different cell lines. We investigated the effect of nonfractionated cigarette smoke extract (CSE) on protein carbonylation in human THP-1 cells. Cells were exposed to various concentrations (2.5-20%) of CSE for 30 min, and protein carbonylation was assessed by use of the sensitive 2,4-dinitrophenylhydrazine immuno-dot blot assay. CSE-induced protein carbonylation exhibited a dose-response relation with CSE concentrations. However, with prolonged exposure to CSE, significant decrements were observed when compared with the 30 min exposure. Cotreatment of THP-1 cells with antioxidants (N-acetyl-cysteine, S-allyl-cysteine, and R-tocopherol) and copper(II) ion chelators (D-penicillamine) during CSE exposure significantly reduced protein carbonylation, whereas cotreatment with antioxidants (vitamin C and trolox) and a metal chelator (EDTA), iron chelator (1,10-phenanthroline), or copper(I) chelator (neocuprin) did not decrease CSE-induced protein carbonylation in THP-1 cells. These results suggest that protein carbonylation is induced by CSE in THP-1 cells via a copper(II)-catalyzed reaction and not an iron-catalyzed reaction. Furthermore, the copper(II) ions involved in this CSE-induced protein carbonylation are derived from the intracellular pool, not via uptake from the extracellular medium. We speculate that natural copper(II) chelators may prevent some of the health problems caused by cigarette smoking, including lung disease, renal failure, and diabetes. © 2009 American Chemical Society.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/18055 http://dx.doi.org/10.1021/tx900008h
Relation:	Chemical Research in Toxicology 22, 1232-1238
Appears in Collections:	[生物醫學科學學系暨碩士班] 期刊論文

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