Abstract
DNA damage prevention is an important mechanism involved in cancer prevention by dietary compounds. Armoracia rusticana is cultivated mainly for its roots that are used in the human diet as a pungent spice. The roots represent rich sources of biologically active phytocompounds, which are beneficial for humans. In this study we investigated the modulation of H2O2 genotoxicity using the A. rusticana root aqueous extract (AE) and two flavonoids (kaempferol or quercetin). Human lymphocytes pre-treated with AE, kaempferol and quercetin were challenged with H2O2 and the DNA damage was assessed by the comet assay. At first we assessed a non-genotoxic concentration of AE and flavonoids, respectively. In lymphocytes challenged with H2O2 we proved that the 0.0025 mg·mL−1 concentration of AE protected human DNA. It significantly reduced H2O2-induced oxidative damage (from 78% to 35.75%). Similarly, a non-genotoxic concentration of kaempferol (5 μg·mL−1) significantly diminished oxidative DNA damage (from 83.3% to 19.4%), and the same concentration of quercetin also reduced the genotoxic effect of H2O2 (from 83.3% to 16.2%). We conclude that AE, kaempferol and quercetin probably act as antimutagens. The molecular mechanisms underlying their antimutagenic activity might be explained by their antioxidant properties.
Highlights
The human body and cells are daily exposed to negative effects of many DNA damaging agents from food or the environment, such as ultraviolet or ionizing radiation, viruses, alkylating or oxidative agents
We wanted to test whether the pre-incubation of lymphocytes with the A. rusticana extract or flavonoids can decrease the hydrogen peroxide-induced DNA damage
We demonstrated that the aqueous extract from A. rusticana and the flavonoids kaempferol and quercetin prevented the induction of single-strand DNA breaks
Summary
The human body and cells are daily exposed to negative effects of many DNA damaging agents from food or the environment, such as ultraviolet or ionizing radiation, viruses, alkylating or oxidative agents These agents can cause DNA damage (single- or double-strand breaks representing primary DNA lesions leading to a fixation of mutations through misrepair or misreplication). When reduction mechanisms are not sufficient, hydrogen peroxide can react with transition metals (iron, copper) and via the Fenton reaction they together produce highly reactive hydroxyl radical which attacks DNA at the sugar residue of the DNA backbone, and this leads to DNA single-strand breaks. Reactive oxygen species (e.g., hydrogen peroxide, superoxide radical, etc.) can cause oxidative damage that negatively influences the function of proteins, induces mutations in nucleic acid and causes lipid peroxidation [3]
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