Prooxidant activity of curcumin: copper-dependent formation of 8-hydroxy-2'-deoxyguanosine in DNA and induction of apoptotic cell death.

@article{Yoshino2004ProoxidantAO,
  title={Prooxidant activity of curcumin: copper-dependent formation of 8-hydroxy-2'-deoxyguanosine in DNA and induction of apoptotic cell death.},
  author={Masataka Yoshino and Miyako Haneda and Makoto Naruse and Hla Hla Htay and Ryoko Tsubouchi and Shanshan Qiao and Wei Hua Li and Keiko Murakami and Takashi. Yokochi},
  journal={Toxicology in vitro : an international journal published in association with BIBRA},
  year={2004},
  volume={18 6},
  pages={
          783-9
        }
}
  • M. Yoshino, M. Haneda, T. Yokochi
  • Published 1 December 2004
  • Biology, Chemistry
  • Toxicology in vitro : an international journal published in association with BIBRA
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Hydroxycinnamic acids as DNA-cleaving agents in the presence of Cu(II) ions: mechanism, structure-activity relationship, and biological implications.
TLDR
It is proposed that it is the CaA phenolate anion that chelates with the Cu(II) ion as a bidentate ligand, hence facilitating the intramolecular electron transfer to form the corresponding CaA semiquinone radical intermediate.
CURCUMIN AND APOPTOSIS: RELATED TO OXIDATIVE STRESS, CARCINOGENESIS AND PROTEASOME INHIBITION
TLDR
In HL-60 cells, inhibition of proteasome mediated proteolysis by specific proteasomal inhibitors, such as curcumin, leads to induction of apoptosis, whereas, lactacystin prolongs survival of nerve growth factor-deprived neuronal apoptosis.
Hexamethoxylated Monocarbonyl Analogues of Curcumin Cause G2/M Cell Cycle Arrest in NCI-H460 Cells via Michael Acceptor-Dependent Redox Intervention.
TLDR
In this study, compounds 1 and 2 were identified as the G2/M cell cycle arrest agents to mediate the cytotoxicity toward NCI-H460 cells via Michael acceptor-dependent redox intervention and provided useful information for understanding the action mechanisms of curcumin and its active analogues.
DNA damage in mouse lymphocytes exposed to curcumin and copper
TLDR
The results show that 50 μM curcumin in the presence of 100–200 μM copper induced DNA damage in murine lymphocytes, andCurcumin alone was capable of inducing DNA strand breaks under the tested conditions.
Curcumin-induced GADD153 gene up-regulation in human colon cancer cells.
TLDR
It is suggested that curcumin-induced up-regulation of GADD153 mRNA expression was at the level of transcription, but apparently without depending on upstream MAPK, in determining the involvement of reactive oxygen species in mediating the effect ofCurcumin on Gadd153.
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TLDR
Treatment of calf thymus DNA with these flavonoids or ascorbate plus copper produced 8-hydroxy-2'-deoxyguanosine and Mutagenic and carcinogenic action of flavonoid may be explained by the prooxidant effects of the compounds.
Strand scission in DNA induced by dietary flavonoids: role of Cu(I) and oxygen free radicals and biological consequences of scission
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The strand scission reaction was shown to account for the biological activity of quercetin as assayed by bacteriophage inactivation and a mechanism for the DNA strand scissions reaction of quERCetin and related flavonoids is proposed.
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It is suggested that gallic acid compounds with hydrophobic chains may enter the cell, and can generate reactive oxygen species through the redox cycling in cells, resulting in the induction of apoptosis.
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TLDR
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