Carbon nanotubes (CNTs) are nanoscale tube-shaped carbon materials used in many industrial areas. Their fiber shape has caused concerns about their toxicity given its structural similarity with asbestos. The aim was to elucidate the effect of CNTs and asbestos exposure on global DNA and RNA methylation as well as on the methylation of genes associated with cell cycle, inflammation and DNA damage processes in human lung cells. Human bronchial epithelial cells (16HBE14o-) were exposed for 24 hours to 25 and 100 µg/ml of CNTs (singlewalled; SWCNTs and multi-walled; MWCNTs) and 2.5 µg/ml of asbestos (chrysotile, amosite, crocidolite) Global DNA and RNA (hydroxy)methylation to cytosines were measured by a validated liquid chromatography tandem-mass spectrometry method (LC-MS/MS). Global RNA methylation to adenines were measured by colorimetric ELISA-like assay. Gene specific DNA methylation status at certain Cytosine-phosphate-Guanine (CpG) sites of cyclin dependent kinase inhibitor 1A, CDKN1A; serine/threonine kinase, ATM; and TNF receptor associated factor 2, TRAF2 were analyzed using bisulfite pyrosequencing technology.Significant global DNA hypomethylation on cytosine and global RNA hypomethylation on
High incidence and poor prognosis of lung cancer make it a major health problem worldwide. Although smoking is a major cause of lung cancer, only some smokers develop lung cancer, which suggests that there is a genetic predisposition in some individuals. 8-OHG is an important oxidative base lesion and may elevate due to cancer and smoking. It is repaired by 8-hydroxyguanine DNA glycosylase 1 (OGG1), which has several polymorphisms. Although the Ser326Cys polymorphism is consistently associated with a range of cancers, findings about this polymorphism and lung cancer risk are contradictory. To date, no study has examined this association in the Turkish population. We conducted a case-control study to investigate the association between OGG1 Ser326Cys polymorphism and the risk of lung cancer using PCR-RFLP. We also evaluated gene-smoking interaction and excretion of urinary 8-OHdG. Our results suggest that the OGG1 Ser326Cys polymorphism is not a genetic risk factor for lung cancer, and that the heterozygous genotype is associated with a significantly reduced risk for lung cancer. The levels of 8-OHdG did not correlate with the polymorphism and smoking. Larger association studies are needed to validate our findings, and mechanistic studies are needed to elucidate the underlying molecular mechanisms of this association.
Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are synthetic chemicals that have been used in industry and consumer products. Because the presence of PFAS has been identified in humans and the environment in the last decade, human exposure to PFAS is a current public health concern. It has been shown that some PFAS lead to adverse health effects in the male reproductive system. However, there is no information about probable genotoxic effects of these chemicals on sperm cells. This study aimed to investigate the possible genotoxic damage on human sperm cells exposed to certain major PFAS compounds that were selected considering their extensive usage, high persistence in the environment, and high bioaccumulation in humans. These PFAS are perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorohexanoic acid (PFHxA). The alkaline comet assay was used to detect the DNA damage to sperm. Sperm cells were treated with 0.1-1 mM of each PFAS at 32 C for 1 h to obtain optimal survival. As a result of the experiments, it was discovered that the exposure to PFOS, PFOA, PFNA, and PFHxA did not cause significant levels of cytotoxicity and did not cause damage to sperm DNA under these conditions. The results suggest that the exposure to these PFAS did not interfere with sperm DNA. Indirect toxicity mechanisms should be taken into account to assess the association between the PFAS exposure and male reproductive toxicity.
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