Chapters authored
The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation
Part of the book: Selected Topics in DNA Repair
Assessment of DNA Damage by Comet Assay in Buccal Epithelial Cells: Problems, Achievement, Perspectives
DNA damage risk assessment in comet assay by the use of buccal mucosa cells has great advantages in comparison with other cell type sample due to more safely, easier, cheaper, and non-invasive method for in vivo studies. According to the OECD Guidelines, the in vivo mammalian alkaline comet assay is well-established and validated method for measuring DNA strand breaks in single eukaryotic cells. Considering exposure to xenobiotics and endogenous damage inductors, buccal mucosa cells are the first to be in direct contact after exposure and this makes them an ideal biomatrices in evaluation of the level of individual genotoxicity to several compounds already mentioned. Their clinical diagnostic applicability confers a potential use in patients across time. However, the number of publications referring to the human buccal comet assay is low in the last two decades. This low growing interest may be explained by several factors, including its relative technical problems. Different procedures have been used in collecting and processing the samples. In order to have widespread acceptance and credibility in human population studies, the comet assay in buccal cells requires standardization of the protocol, of parameters analyzed, and a better knowledge of critical features affecting the assay outcomes, including the definition of the values of spontaneous DNA damage. There is a need for further collaborative work as in the HUMN (micronucleus assay on lymphocytes) and HUMNxL (micronucleus assay on buccal cells) collaborative projects. The creation of a network of laboratories will allow more focused validation studies, including the design of a classic, historic, prospective cohort study in order to explore the link between measures of genetic instability in the buccal mucosa and the risk of cancer and other chronic-degenerative diseases. One such network connection will start in 2016 as a COST project under the name “hCOMET—The comet assay as a human biomonitoring tool” launched by Prof. Andrew Collins.
Part of the book: Environmental Health Risk
DNA Damage and Glutathione Peroxidase Activity in Liver and Kidney Cells in Wistar Rats Exposed to Terbuthylazine (TERB) for 28 Consecutive Days
The potential of low doses of the chloro-triazine herbicide terbuthylazine to induce DNA damage and impair activity of glutathione peroxidase (GPx) was evaluated in kidney and parenchymal and non-parenchymal liver cells of adult male rats. In a 28-day study, terbuthylazine was applied daily by oral gavage at doses: 0.004, 0.4 and 2.29 mg/kg bw/day. Tail Intensity (T Int) and Tail Length (TL) were used as descriptors of DNA damage. In the kidney, Tail Int was significantly different in all treated groups, while TL was different in 0.4 and 2.29 mg/kg bw/day groups, compared to controls. Significant differences in TL were recorded in parenchymal and non-parenchymal liver cells of all treated groups. Tail Int was significantly different from controls in non-parenchymal liver cells at all applied doses and in parenchymal cells at terbuthylazine doses of 0.004 and 2.29 mg/kg bw/day. A significant increase in GPx activity was observed only in the kidney at doses 0.4 and 2.29 mg/kg bw/day compared to the controls indicating its possible role in the protection of kidney from free radicals. It appears that repeated exposure to low doses of terbuthylazine could cause DNA instability in kidney cells and in parenchymal and non-parenchymal liver cells in rats.
Part of the book: Rodents