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Mitochondria-Accumulating Rhenium(I) Tricarbonyl ComplexesInduce Cell Death via Irreversible Oxidative Stress and GlutathioneMetabolism Disturbance

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Penulis : Fang-Xin Wang [-]
Kontributor / Dosen Pembimbing :
  • Jin-Hao Liang, Hang Zhang, Ze-Hua Wang, Qin Wan, Cai-Ping Tan,Liang-Nian Ji,and Zong-Wan Mao
Jenis Koleksi : Jurnal elektronik
Tahun Terbit :
Penerbit : Kimia
Fakultas : Fakultas Matematika dan Ilmu Pengetahuan Alam
Subjek : Chemistry
Kata Kunci : rhenium(I) complexes, apoptosis, necroptosis, mitochondrial dysfunction, oxidative stress, glutathione metabolism
Sumber : ACS Appl. Mater. InterfacesXXXX, XXX, XXX?XXX
Staf Input/Edit : Latifa Noor  
File : 1 file
Tanggal Input : 02 Apr 2019

Mitochondria play a critical role in tumorigenesis.Targeting mitochondria and disturbing related events have beenemerging as a promising way for chemotherapy. In this work, twobinuclear rhenium(I) tricarbonyl complexes of the general formula[Re2(CO)6(dip)2L](PF6)2(dip = 4,7-diphenyl-1,10-phenanthroline; L =4,4?-azopyridine (ReN) or 4,4?-dithiodipyridine (ReS)) were synthesizedand characterized.ReNandReScan react with glutathione (GSH). Theyexhibit good in vitro anticancer activity against cancer cell lines screened.Besides, they can target mitochondria, cause oxidative stress, and disturbGSH metabolism. BothReNandReScan induce necroptosis andcaspase-dependent apoptosis simultaneously. We also demonstrate thatReNandReScan inhibit tumor growth in nude mice bearing carcinomaxenografts. Our study shows the potential of Re(I) complexes aschemotherapeutic agents to kill cancer cells via a mitochondria-to-cellularredox strategy.

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