Vitamin C for DNA damage prevention

Radim J Sram1, Blanka Binkova, Pavel Rossner

  • 1Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14220 Prague 4, Czech Republic. sram@biomed.cas.cz

Mutation Research
|December 20, 2011
PubMed

Insights

Vitamin C protects against genetic damage by reducing DNA adducts, chromosomal aberrations, and oxidative stress. Optimal protection is observed at plasma vitamin C levels exceeding 50 μmol/l, particularly in exposed populations.

Area of Science:

  • Molecular epidemiology
  • Nutritional science
  • Genetics

Background:

  • Genetic damage can arise from environmental exposures and oxidative stress.
  • Vitamin C (ascorbic acid) is a potent antioxidant with potential protective roles against DNA damage.

Purpose of the Study:

  • To review human studies on vitamin C's effects on genetic damage using molecular epidemiology.
  • To identify specific types of DNA damage influenced by vitamin C and effective plasma concentrations.

Main Methods:

  • Analysis of DNA adducts, DNA strand breakage (Comet assay), and oxidative damage (8-oxodG).
  • Cytogenetic analysis including chromosomal aberrations and micronuclei.
  • Assessment of DNA repair protein induction and sensitivity to mutagens (bleomycin assay).

Main Results:

  • Vitamin C demonstrated protective effects against various DNA damages, including chromosomal aberrations, genomic translocations, micronuclei, DNA adducts, strand breakage, and oxidative damage (8-oxodG).
  • These effects were particularly noted at plasma vitamin C levels >50 μmol/l.
  • Supplementation was beneficial for individuals with insufficient dietary intake, smokers, and those exposed to mutagens, ionizing radiation, air pollution (c-PAHs, PM2.5).

Conclusions:

  • Vitamin C exhibits significant protective effects against environmentally induced genetic damage.
  • Adequate plasma levels of vitamin C are crucial for mitigating DNA damage from xenobiotics and oxidative stress.
  • The impact of vitamin C may depend on individual baseline levels and exposure intensity.

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