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Assessing dose-dependent differences in DNA-damage, p53 response and genotoxicity for quercetin and curcumin

Bin Sun1, Susan M Ross, O Joseph Trask

  • 1The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, USA.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|June 15, 2013
PubMed

Insights

Curcumin and quercetin are natural compounds that trigger DNA damage responses differently. Curcumin is more potent, causing reactive oxygen species and DNA damage at lower doses than quercetin, leading to distinct cellular effects.

Area of Science:

  • Cellular and Molecular Biology
  • Toxicology
  • Pharmacology

Background:

  • The p53-Mdm2 pathway is crucial for cellular response to DNA damage.
  • Natural compounds like quercetin (QUE) and curcumin (CUR) are investigated for their effects on this pathway.
  • Understanding dose-response relationships is vital for assessing potential health impacts of these polyphenols.

Purpose of the Study:

  • To compare the dose-dependent DNA damage response of quercetin and curcumin in HT1080 cells.
  • To investigate the differential effects of these compounds on reactive oxygen species, DNA damage biomarkers, and cell cycle progression.
  • To inform the development of a quantitative mechanistic model of the p53-Mdm2 DNA-damage pathway.

Main Methods:

  • Exposure of HT1080 human cells (wild-type p53) to varying doses of QUE and CUR.
  • Measurement of reactive oxygen species (ROS) production.
  • Assessment of DNA damage via phospho-H2AX (γ-H2AX) levels.
  • Quantification of p53 induction.
  • Analysis of cell cycle distribution (S phase and G2/M arrest).
  • Evaluation of apoptosis induction.
  • Determination of micronuclei frequency as a genotoxicity biomarker.

Main Results:

  • Curcumin (CUR) was more potent than quercetin (QUE) in inducing ROS, DNA damage (γ-H2AX), and p53. Lowest observed effect levels (LOELs) for CUR were 3-8 μM, while for QUE they were 20-30 μM.
  • CUR induced significant G2/M arrest and apoptosis at approximately 10 μM, whereas QUE caused S phase arrest at 8 μM and apoptosis only at much higher doses (60 μM).
  • At comparable levels of p-H2AX and p53, CUR induced a greater frequency of micronuclei than QUE, with clear increases observed at 3-6 μM for CUR and a weaker response for QUE even at highest doses.

Conclusions:

  • Quercetin and curcumin exhibit distinct dose-response patterns and cellular effects despite shared chemical properties.
  • Curcumin demonstrates higher potency in initiating DNA damage responses and driving cell fate decisions (arrest, apoptosis) at lower concentrations compared to quercetin.
  • These findings highlight the importance of dose and compound-specific mechanisms in evaluating the genotoxic and cytotoxic potential of natural polyphenols.
Keywords:
CurcuminDNA damageDNA repairMicronucleusPolyphenolsQuercetinp53

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