Apoptosis induced by para-phenylenediamine involves formation of ROS and activation of p38 and JNK in chang liver cells

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Title:	Apoptosis induced by para-phenylenediamine involves formation of ROS and activation of p38 and JNK in chang liver cells
Authors:	陳師慶;Chye, Soi Moi;Tiong, Yee Lian;Yip, Wai Kien;Koh, Rhun Yian;Len, Yi Won;Seow, Heng Fong;Ng, Khuen Yen;Ranjit, De Alwis;Chen, Ssu Ching
Contributors:	生醫理工學院生命科學系
Keywords:	apoptosis;Apoptosis - drug effects;cell cycle;Cell Line;cell viability;Chang liver cells;cytology;Cytotoxicity;DNA damage;drug effects;dyes;Enzyme Activation;enzymology;flow cytometry;growth retardation;hepatocytes;Humans;Imidazoles;Imidazoles - pharmacology;Liver;Liver - cytology;Liver - drug effects;Liver - enzymology;MAP Kinase Kinase 4;MAP Kinase Kinase 4 - metabolism;MAP-kinases;metabolism;mitogen-activated protein kinase;p38 Mitogen-Activated Protein Kinases;p38 Mitogen-Activated Protein Kinases - metabolism;para-phenylenediamine;pharmacology;Phenylenediamines;Phenylenediamines - pharmacology;Phosphorylation;Pyridines;Pyridines - pharmacology;reactive oxygen species;Western blotting
Date:	2014-01-01
Issue Date:	2026-04-23 11:11:37 (UTC+8)
Publisher:	John Wiley and Sons Inc.;United States: John Wiley & Sons
Abstract:	摘要： para‐phenylenediamine (p‐PD) is a suspected carcinogen, but it has been widely used as a component in permanent hair dyes. In this study, the mechanism of p‐PD‐induced cell death in normal Chang liver cells was investigated. The results demonstrated that p‐PD decreased cell viability in a dose‐dependent manner. Cell death via apoptosis was confirmed by enhanced DNA damage and increased cell number in the sub‐G1 phase of the cell cycle, using Hoechst 33258 dye staining and flow cytometry analysis. Apoptosis via reactive oxygen species generation was detected by the dichlorofluorescin diacetate staining method. Mitogen‐activated protein kinase (MAPK) activation was assessed by western blot analysis and revealed that p‐PD activated not only stress‐activated protein kinase (SAPK)/c‐Jun N‐terminal kinases (JNK) and p38 MAPK but also extracellular signal‐regulated kinase (ERK). Cytotoxicity and apoptosis induced by p‐PD were markedly enhanced by ERK activation and selectively inhibited by ERK inhibitor PD98059, thus indicating a negative role of ERK. In contrast, inhibition of p38 MAPK activity with the p38‐specific inhibitor SB203580 moderately inhibited cytotoxicity and apoptosis induction by p‐PD. Similarly, SP600125, an inhibitor of SAPK/JNK, moderately inhibited cytotoxicity and apoptosis induced by p‐PD, thus implying that p38 MAPK and SAPK/JNK had a partial role in p‐PD‐induced apoptosis. Western blot analysis revealed that p‐PD significantly increased phosphorylation of p38 and SAPK/JNK and decreased phosphorylation of ERK. In conclusion, the results demonstrated that SAPK/JNK and p38 cooperatively participate in apoptosis induced by p‐PD and that a decreased ERK signal contributes to growth inhibition or apoptosis. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 981–990, 2014. 其他題名： Environ. Toxicol 出版者： United States: John Wiley & Sons 出版日期： 2014-09 出處： Environmental toxicology, 2014-09, Vol.29 (9), p.981-990 資源來源： Wiley Journals Core Collection (NTUSG) 版權： Copyright © 2012 Wiley Periodicals, Inc., a Wiley company 版權： Copyright © 2012 Wiley Periodicals, Inc., a Wiley company. 識別號： ISSN: 1520-4081 識別號： ISSN: 1522-7278 識別號： EISSN: 1522-7278 識別號： DOI: 10.1002/tox.21828 識別號： PMID: 23172806 識別號： CODEN: ETOXFH
Appears in Collections:	[Department of Life Science] journal & Dissertation

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