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Article: A novel synthetic compound, bismuth zinc citrate, could potentially reduce cisplatin-induced toxicity without compromising the anticancer effect through enhanced expression of antioxidant protein

TitleA novel synthetic compound, bismuth zinc citrate, could potentially reduce cisplatin-induced toxicity without compromising the anticancer effect through enhanced expression of antioxidant protein
Authors
Issue Date2019
PublisherElsevier: Creative Commons Attribution Non-Commercial No-Derivatives License. The Journal's web site is located at http://www.transonc.com
Citation
Translational Oncology, 2019, v. 12, p. 788-799 How to Cite?
AbstractCisplatin is a common anticancer drug, but it comes with significant nephrotoxicity. Further cisplatin-induced oxidative stress contributes to the pathogenesis of the nephrotoxicity. A new compound, BiZn, can potentially prevent this complication. We verified our postulation by in vitro and in vivo models. From our findings, BiZn did not affect cisplatin-induced cytotoxicity on neuroblastoma cells under both in vitro and in vivo settings. However, BiZn significantly reduced the blood urea nitrogen and creatinine levels in cisplatin-treated mice. Under the lethal dosage of cisplatin, co-treatment of BiZn significantly increased the survival rate. BiZn stimulated antioxidant proteins metallothionein (MT) and glutathione (GSH) generation from kidney cells and minimized cisplatin-induced apoptosis. Knocking down MT-IIA and inhibiting GSH abolished such protection. In conclusion, pretreatment of BiZn decreased cisplatin-induced renal toxicity without affecting its antitumor activity. BiZn-induced antioxidant proteins MT and GSH may contribute to the renal protection effect.
Persistent Identifierhttp://hdl.handle.net/10722/270076
ISSN
2015 Impact Factor: 3.077

 

DC FieldValueLanguage
dc.contributor.authorChan, S-
dc.contributor.authorWang, R-
dc.contributor.authorMan, K-
dc.contributor.authorNicholls, JM-
dc.contributor.authorLi, H-
dc.contributor.authorSun, H-
dc.contributor.authorChan, GCF-
dc.date.accessioned2019-05-20T05:09:02Z-
dc.date.available2019-05-20T05:09:02Z-
dc.date.issued2019-
dc.identifier.citationTranslational Oncology, 2019, v. 12, p. 788-799-
dc.identifier.issn1944-7124-
dc.identifier.urihttp://hdl.handle.net/10722/270076-
dc.description.abstractCisplatin is a common anticancer drug, but it comes with significant nephrotoxicity. Further cisplatin-induced oxidative stress contributes to the pathogenesis of the nephrotoxicity. A new compound, BiZn, can potentially prevent this complication. We verified our postulation by in vitro and in vivo models. From our findings, BiZn did not affect cisplatin-induced cytotoxicity on neuroblastoma cells under both in vitro and in vivo settings. However, BiZn significantly reduced the blood urea nitrogen and creatinine levels in cisplatin-treated mice. Under the lethal dosage of cisplatin, co-treatment of BiZn significantly increased the survival rate. BiZn stimulated antioxidant proteins metallothionein (MT) and glutathione (GSH) generation from kidney cells and minimized cisplatin-induced apoptosis. Knocking down MT-IIA and inhibiting GSH abolished such protection. In conclusion, pretreatment of BiZn decreased cisplatin-induced renal toxicity without affecting its antitumor activity. BiZn-induced antioxidant proteins MT and GSH may contribute to the renal protection effect.-
dc.languageeng-
dc.publisherElsevier: Creative Commons Attribution Non-Commercial No-Derivatives License. The Journal's web site is located at http://www.transonc.com-
dc.relation.ispartofTranslational Oncology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleA novel synthetic compound, bismuth zinc citrate, could potentially reduce cisplatin-induced toxicity without compromising the anticancer effect through enhanced expression of antioxidant protein-
dc.typeArticle-
dc.identifier.emailChan, S: schan88@hkucc.hku.hk-
dc.identifier.emailWang, R: u3002771@connect.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.emailNicholls, JM: jmnichol@hkucc.hku.hk-
dc.identifier.emailLi, H: hylichem@hku.hk-
dc.identifier.emailSun, H: hsun@hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.authorityNicholls, JM=rp00364-
dc.identifier.authoritySun, H=rp00777-
dc.identifier.authorityChan, GCF=rp00431-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.tranon.2019.02.003-
dc.identifier.hkuros297872-
dc.identifier.volume12-
dc.identifier.spage788-
dc.identifier.epage799-
dc.publisher.placeUnited States-

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