The first copper(ii) complex with 1,10-phenanthroline and salubrinal with interesting biochemical properties
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
32337526
DOI
10.1039/d0mt00006j
Knihovny.cz E-resources
- MeSH
- Antiviral Agents pharmacology MeSH
- Cinnamates pharmacology MeSH
- Phenanthrolines pharmacology MeSH
- Taurochenodeoxycholic Acid pharmacology MeSH
- Humans MeSH
- Magnetic Resonance Spectroscopy MeSH
- Copper pharmacology MeSH
- Molecular Structure MeSH
- Cell Line, Tumor MeSH
- Lipid Peroxidation drug effects MeSH
- DNA Damage drug effects genetics MeSH
- Thiourea analogs & derivatives pharmacology MeSH
- Transcription Factor CHOP genetics metabolism MeSH
- Microscopy, Electron, Transmission MeSH
- Cell Survival drug effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 1,10-phenanthroline MeSH Browser
- Antiviral Agents MeSH
- Cinnamates MeSH
- Phenanthrolines MeSH
- Taurochenodeoxycholic Acid MeSH
- Copper MeSH
- salubrinal MeSH Browser
- Thiourea MeSH
- Transcription Factor CHOP MeSH
- ursodoxicoltaurine MeSH Browser
The novel copper complex [Cu(phen)2(salubrinal)](ClO4)2 (C0SAL) has been synthesised and characterised. Copper(ii) is coordinated by salubrinal through the thionic group, as shown by the UV-Vis, IR, ESI-MS and tandem mass results, together with the theoretical calculations. The formed complex showed a DPPH radical scavenging ability higher than that of salubrinal alone. Studies on lipid oxidation inhibition showed that the C0SAL concentration, required to inhibit the enzyme, was lower than that of salubrinal. The inhibition of the enzyme could take place via allosteric modulation, as suggested by docking calculations. C0SAL showed a good cytotoxic activity on A2780 cells, 82 fold higher than that of the precursor salubrinal and 1.4 fold higher than that of [Cu(phen)2(H2O)](ClO4)2. Treatment with C0SAL in SKOV3 ovarian cancer cells induced expression of GRP-78 and DDIT3 regulators of ER-stress response. The cytotoxic effect of C0SAL was reverted in the presence of TUDCA, suggesting that C0SAL induces cell death through ER-stress. In A2780 cells treated with C0SAL γ-H2AX was accumulated, suggesting that DNA damage was also involved.
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