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Article: Bismuth Porphyrin Antagonizes Cisplatin-Induced Nephrotoxicity via Unexpected Metallothionein-Independent Mechanisms

TitleBismuth Porphyrin Antagonizes Cisplatin-Induced Nephrotoxicity via Unexpected Metallothionein-Independent Mechanisms
Authors
KeywordsInorganic Chemistry
Medical Biochemistry
Organometallic Chemistry
Issue Date2020
PublisherCell Press. The Journal's web site is located at https://www.cell.com/iscience.home
Citation
iScience, 2020, v. 23 n. 5, p. article no. 101054 How to Cite?
AbstractSummary: Cisplatin (CDDP) has been a highly successful anticancer drug in cancer therapy; however, its further application suffers severe nephrotoxicity. Herein, we identify bismuth tetraphenylporphyrinate [Bi(TPP)] as a potent protective agent against CDDP-induced nephrotoxicity. Bi(TPP) attenuates CDDP-induced acute kidney injury and prevents the death of mice exposed to a lethal dose of CDDP. The protective potency of bismuth porphyrin complexes could be optimized by varying lipophilic TPP ligands with ideal ClogP values of 8–14. Unexpectedly, Bi(TPP) exhibited a protective role via metallothionein-independent pathways, i.e., maintenance of redox homeostasis and energy supplement, elimination of accumulated platinum in the kidney, and inactivation of caspases cascade in apoptotic pathway. Significantly, Bi(TPP) does not compromise the antitumor activity of CDDP in the orthotopic tumor xenograft mouse model. These findings suggest that Bi(TPP) could be incorporated into current CDDP-based cancer therapy as a nephroprotective agent.
Persistent Identifierhttp://hdl.handle.net/10722/286169
ISSN
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWang, R-
dc.contributor.authorWANG, S-
dc.contributor.authorChan, S-
dc.contributor.authorWang, Y-
dc.contributor.authorZhang, Y-
dc.contributor.authorZuo, Z-
dc.contributor.authorChan, GCF-
dc.contributor.authorLi, H-
dc.contributor.authorSun, H-
dc.date.accessioned2020-08-31T07:00:06Z-
dc.date.available2020-08-31T07:00:06Z-
dc.date.issued2020-
dc.identifier.citationiScience, 2020, v. 23 n. 5, p. article no. 101054-
dc.identifier.issn2589-0042-
dc.identifier.urihttp://hdl.handle.net/10722/286169-
dc.description.abstractSummary: Cisplatin (CDDP) has been a highly successful anticancer drug in cancer therapy; however, its further application suffers severe nephrotoxicity. Herein, we identify bismuth tetraphenylporphyrinate [Bi(TPP)] as a potent protective agent against CDDP-induced nephrotoxicity. Bi(TPP) attenuates CDDP-induced acute kidney injury and prevents the death of mice exposed to a lethal dose of CDDP. The protective potency of bismuth porphyrin complexes could be optimized by varying lipophilic TPP ligands with ideal ClogP values of 8–14. Unexpectedly, Bi(TPP) exhibited a protective role via metallothionein-independent pathways, i.e., maintenance of redox homeostasis and energy supplement, elimination of accumulated platinum in the kidney, and inactivation of caspases cascade in apoptotic pathway. Significantly, Bi(TPP) does not compromise the antitumor activity of CDDP in the orthotopic tumor xenograft mouse model. These findings suggest that Bi(TPP) could be incorporated into current CDDP-based cancer therapy as a nephroprotective agent.-
dc.languageeng-
dc.publisherCell Press. The Journal's web site is located at https://www.cell.com/iscience.home-
dc.relation.ispartofiScience-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectInorganic Chemistry-
dc.subjectMedical Biochemistry-
dc.subjectOrganometallic Chemistry-
dc.titleBismuth Porphyrin Antagonizes Cisplatin-Induced Nephrotoxicity via Unexpected Metallothionein-Independent Mechanisms-
dc.typeArticle-
dc.identifier.emailWang, R: chemrmw@HKUCC-COM.hku.hk-
dc.identifier.emailChan, S: schan88@hkucc.hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.emailSun, H: sunhui@hku.hk-
dc.identifier.authorityChan, GCF=rp00431-
dc.identifier.authoritySun, H=rp00778-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.isci.2020.101054-
dc.identifier.pmid32353763-
dc.identifier.pmcidPMC7191608-
dc.identifier.scopuseid_2-s2.0-85083717291-
dc.identifier.hkuros313742-
dc.identifier.volume23-
dc.identifier.issue5-
dc.identifier.spagearticle no. 101054-
dc.identifier.epagearticle no. 101054-
dc.publisher.placeUnited States-

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