Regular ArticleN-Nitrosodimethylamine-Mediated Cytotoxicity in a Cell Line Expressing P450 2E1: Evidence for Apoptotic Cell Death
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Dioscin alleviates dimethylnitrosamine-induced acute liver injury through regulating apoptosis, oxidative stress and inflammation
2016, Environmental Toxicology and PharmacologyCitation Excerpt :Inflammation plays an important role in DMN-induced acute liver injury. ROS produced by DMN not only directly causes liver injury, but also initiates inflammation (Lin et al., 1999). TLR4, an important pattern recognition receptor (PRR), can activate NF-κB pathway by combining with MyD88, increase the degradation of IκBɑ, thus promote the translocation of NF-κBp50 and p65 into nucleus.
Genotoxic evaluation of the non-halogenated disinfection by-products nitrosodimethylamine and nitrosodiethylamine
2011, Journal of Hazardous MaterialsCitation Excerpt :To investigate if these nitrosamines are able to produce oxidative DNA damage, we evaluated the effectiveness of NDMA and NDEA in inducing this kind of damage by using endoIII and FPG treatments. Reactive oxygen species may partially contribute to the genotoxic effect of NDMA, as observed in P450 2E1-expressing cells [44,46]. Our results show that only the FPG treatment enhances the DNA damage produced by NDMA and NDEA, indicating that only oxidized purines are induced.
Evaluation of the genotoxicity of 10 selected dietary/environmental compounds with the in vitro micronucleus cytokinesis-block assay in an interlaboratory comparison
2010, Food and Chemical ToxicologyCitation Excerpt :Carcinogenesis can also be triggered at organ specific sites as observed in rat liver (Fournier, 1990). NDMA requires metabolic activation to exert its biological effects (Fournier, 1990) and generates metabolites which trigger apoptosis (Lin et al., 1999). In turn, this can be accompanied with presence of ROS (Jablonski et al., 2001).
A cell-microelectronic sensing technique for profiling cytotoxicity of chemicals
2008, Analytica Chimica ActaCitation Excerpt :The various profiles of nitrosamine-dependent and cell line-dependent cytotoxicity that are detected by RT-CES may be related to different factors. For example, specific nitrosamines may require activation by specific P450 isozymes in order to cause toxic effects, and different types of cells may have different levels of P450 expression (Table 2) [29–37]. NDMA, NPyr, and NPip are metabolized by P450 enzymes to form hydroxyl radical intermediates via α-hydroxylation.
CYP2E1 and oxidative liver injury by alcohol
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