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Article: Cytotoxicity induced by iodinated haloacetamides via ROS accumulation and apoptosis in HepG-2 cells

TitleCytotoxicity induced by iodinated haloacetamides via ROS accumulation and apoptosis in HepG-2 cells
Authors
KeywordsApoptosis
Cytotoxicity
HepG-2 cell
Iodinated haloacetamides
Reactive oxygen species (ROS)
Issue Date2018
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/envpol
Citation
Environmental Pollution, 2018, v. 242, p. 191-197 How to Cite?
AbstractIodinated haloacetamides (I-HAcAms) are emerging disinfection by-products and have received great concern due to their extremely high health risk. Previous studies have demonstrated the cytotoxicity of I-HAcAms, but the biological mechanism remained unclear. In this study, cytotoxicity mechanisms of 4 I-HAcAms species were preliminarily examined using HepG-2 cells. The results showed that the cytotoxicity could be ranked as follows: diiodoacetamide (DIAcAm)> iodoacetamide (IAcAm)> bromoiodoacetamide (BIAcAm)> chloroiodoacetamide (CIAcAm). Reactive oxygen species (ROS) and apoptosis played an important role in the cytotoxicity for all I-HAcAms species. Moreover, the ROS and cytotoxicity could be completely reversed by the addition of an antioxidant (N-acetylcysteine (NAC)), but the apoptosis could not. Specifically, the apoptosis induced by DIAcAm and IAcAm was partially reversed by NAC, suggesting that in addition to ROS, other pathways were also possible; While For BIAcAm and CIAcAm, the apoptosis was not reversed by NAC at all, which is potentially due to ROS-independent pathways. The apoptosis mechanisms were further analyzed via Bax and Bcl-2 gene expression and the corresponding protein expression in HepG-2 cells, that mitochondrial pathway was important in the apoptosis of HepG-2 cells induced by all I-HAcAms species. Overall, the mitochondrial pathway provided a potential explanation for BIAcAm and CIAcAm-induced apoptosis, while both ROS and mitochondrial pathways explained DIAcAm and IAcAm-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/261076
ISSN
2019 Impact Factor: 6.792
2015 SCImago Journal Rankings: 2.045
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHong, H-
dc.contributor.authorWu, H-
dc.contributor.authorChen, J-
dc.contributor.authorWu, B-
dc.contributor.authorYu, H-
dc.contributor.authorYan, B-
dc.contributor.authorLiang, Y-
dc.date.accessioned2018-09-14T08:52:05Z-
dc.date.available2018-09-14T08:52:05Z-
dc.date.issued2018-
dc.identifier.citationEnvironmental Pollution, 2018, v. 242, p. 191-197-
dc.identifier.issn0269-7491-
dc.identifier.urihttp://hdl.handle.net/10722/261076-
dc.description.abstractIodinated haloacetamides (I-HAcAms) are emerging disinfection by-products and have received great concern due to their extremely high health risk. Previous studies have demonstrated the cytotoxicity of I-HAcAms, but the biological mechanism remained unclear. In this study, cytotoxicity mechanisms of 4 I-HAcAms species were preliminarily examined using HepG-2 cells. The results showed that the cytotoxicity could be ranked as follows: diiodoacetamide (DIAcAm)> iodoacetamide (IAcAm)> bromoiodoacetamide (BIAcAm)> chloroiodoacetamide (CIAcAm). Reactive oxygen species (ROS) and apoptosis played an important role in the cytotoxicity for all I-HAcAms species. Moreover, the ROS and cytotoxicity could be completely reversed by the addition of an antioxidant (N-acetylcysteine (NAC)), but the apoptosis could not. Specifically, the apoptosis induced by DIAcAm and IAcAm was partially reversed by NAC, suggesting that in addition to ROS, other pathways were also possible; While For BIAcAm and CIAcAm, the apoptosis was not reversed by NAC at all, which is potentially due to ROS-independent pathways. The apoptosis mechanisms were further analyzed via Bax and Bcl-2 gene expression and the corresponding protein expression in HepG-2 cells, that mitochondrial pathway was important in the apoptosis of HepG-2 cells induced by all I-HAcAms species. Overall, the mitochondrial pathway provided a potential explanation for BIAcAm and CIAcAm-induced apoptosis, while both ROS and mitochondrial pathways explained DIAcAm and IAcAm-induced apoptosis.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/envpol-
dc.relation.ispartofEnvironmental Pollution-
dc.subjectApoptosis-
dc.subjectCytotoxicity-
dc.subjectHepG-2 cell-
dc.subjectIodinated haloacetamides-
dc.subjectReactive oxygen species (ROS)-
dc.titleCytotoxicity induced by iodinated haloacetamides via ROS accumulation and apoptosis in HepG-2 cells-
dc.typeArticle-
dc.identifier.emailYan, B: yanbin14@hku.hk-
dc.identifier.authorityYan, B=rp01940-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.envpol.2018.06.090-
dc.identifier.pmid29980037-
dc.identifier.scopuseid_2-s2.0-85049873286-
dc.identifier.hkuros290521-
dc.identifier.volume242-
dc.identifier.spage191-
dc.identifier.epage197-
dc.identifier.isiWOS:000446150300022-
dc.publisher.placeUnited Kingdom-

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