Objective To elucidate the etiology of DNA impairment of type Ⅱ alveolar epithelial cells(AT-II) of the rats fed with low selenium and high cadmium fodder，and the effect of Vitamin C.Methods With single cell gel electrophoresis technique，we observed the joint action of selenium，cadmium and vitamin C on DNA damage in AT-II cells of the eight groups of rats fed separately with：normal （2 groups），high Cd，high Cd+high VC，low Se+high Cd，low Se+high Cd+high VC，high Se+high Cd and high Se+high Cd+high VC fodder for 14 weeks.Results Compared with the control，there was no DNA changes have been observed in the high Se+high Cd+high VC group.However，in the high Se+high Cd group and high Cd+high VC group，DNA damage of AT-II cells can be detected clearly；in the low Se+high Cd+high VC group and high Cd group，the degree of the DNA damage is more serious than the above two groups；in the low Se+high Cd group，the extent of the DNA damage was the most serious on all of the groups be studied.Conclusion It is suggested that Se deficiency and simultaneously Cd overabundance may damaged DNA of AT-II cells of the rats significantly，however，Vitamin C may protect AT-II against the injury effectively.
Cardiovascular disease is a severe threat to human health and life. Among many risk factors of cardiovascular disease, genetic or gene-based ones are drawing more and more attention in recent years. Accumulated evidence has demonstrated that the loss or mutation of ataxia telangiectasia mutated (ATM) gene can result in DNA damage repair dysfunctions, telomere shortening, decreased antioxidant capacity, insulin resistance, increased lipid levels, etc., and thus can promote the occurrence of cardiovascular risk factors, such as aging, atherosclerosis and metabolic syndrome. In this review, we discusses the possible mechanisms between ATM gene and cardiovascular risk factors, which could be helpful to the related research and clinical application.
The deoxyribonucleic acid (DNA) molecule damage simulations with an atom level geometric model use the traversal algorithm that has the disadvantages of quite time-consuming, slow convergence and high-performance computer requirement. Therefore, this work presents a density-based spatial clustering of applications with noise (DBSCAN) clustering algorithm based on the spatial distributions of energy depositions and hydroxyl radicals (·OH). The algorithm with probability and statistics can quickly get the DNA strand break yields and help to study the variation pattern of the clustered DNA damage. Firstly, we simulated the transportation of protons and secondary particles through the nucleus, as well as the ionization and excitation of water molecules by using Geant4-DNA that is the Monte Carlo simulation toolkit for radiobiology, and got the distributions of energy depositions and hydroxyl radicals. Then we used the damage probability functions to get the spatial distribution dataset of DNA damage points in a simplified geometric model. The DBSCAN clustering algorithm based on damage points density was used to determine the single-strand break (SSB) yield and double-strand break (DSB) yield. Finally, we analyzed the DNA strand break yield variation trend with particle linear energy transfer (LET) and summarized the variation pattern of damage clusters. The simulation results show that the new algorithm has a faster simulation speed than the traversal algorithm and a good precision result. The simulation results have consistency when compared to other experiments and simulations. This work achieves more precise information on clustered DNA damage induced by proton radiation at the molecular level with high speed, so that it provides an essential and powerful research method for the study of radiation biological damage mechanism.