The aim of the study was to analyze the level of DNA damage and DNA repair efficiency in peripheral blood lymphocytes of EC patients, taking into account whether or not they had a family history of cancer.
The alkaline comet assay technique was used to quantify the level of DNA damage and the DNA repair in lymphocytes.
The consequences of upsetting this balance by increasing the level of DNA damage or by mutational inactivation of DNA repair genes are highly deleterious and result in the development of cancers in humans and in mouse models [8], [9], [10], [11].
To select the appropriate range of etoposide dosage for activating variable amounts of DNA damage, we first measured the level of DNA damage under different etoposide doses.
The initial distribution of irradiated cells as a function of the comet tail moment, which reflects the level of DNA damage, shows a shift towards a population of more damaged cells, as compared with the sham-irradiated cells.
Thus, by reducing the level of DNA damage signaling, as we presently see, metformin appears to alleviate the extent of the persistent DNA replication stress.
In conclusion, we have demonstrated that dietary HAMSB provides a dose-related reduction in the level of DNA damage and an increase in the rate of apoptotic deletion of damaged colonic epithelial cells after acute treatment with AOM.
SNPs that lead to an increase in the level of DNA damage, (i.e. by increasing the bioactivation of toxins to reactive intermediates), could synergize with impaired DNA repair mechanisms, leading to a greater than additive increase in cancer risk.
Silver nanoparticles had demonstrated antimicrobial activity at the level of DNA damage, cytoplasmic membrane, etc.
After 24 h treatment with ZnO NPs, the level of DNA damage significantly increased at all tested doses (Figure 6B).
Nevertheless, when the DNA damage burden does not exceed the level of DNA damage recognition, transcriptional regulation of respective proteins is not expected.
