In vitro mutagenicity and genotoxicity study of 1,2-dichloroethylene, 1,1,2-trichloroethane, 1,3-dichloropropane, 1,2,3-trichloropropane and 1,1,3-trichloropropene, using the micronucleus test and the alkaline single cell gel electrophoresis technique (comet assay) in human lymphocytes
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Genomic damage induced by the widely used fungicide chlorothalonil in peripheral human lymphocytes
2018, Ecotoxicology and Environmental SafetyCitation Excerpt :Like chlorothalonil, most of these polychlorinated compounds also showed genotoxic properties. For example, 1,2-dichloroethylene, 1,1,2-trichloroethane, 1,3-dichloropropane, and 1,1,3-trichloropropene, widely used as solvents and degreasing agents in industry, were found to induce MNi and DNA damage in human lymphocytes (Tafazoli and Kirsch-Volders, 1996). Similarly, 2,2′,4,4′,5,5′-hexachlorobiphenyl, 2,3′,4,4′,5- and 2,2′,4′,5,5′-pentachlorobiphenyls, were found to induce MNi and DNA breaks in fish RTG-2 cells (Marabini et al., 2011).
Genotoxicity assessment of piperitenone oxide: An in vitro and in silico evaluation
2017, Food and Chemical ToxicologyAssessment of DNA damage, cytotoxicity, and apoptosis in human hepatoma (HepG2) cells after flurochloridone herbicide exposure
2014, Food and Chemical ToxicologyCitation Excerpt :It its known that the difference between results in the SCGE and CBMN-cyt assays is essentially due to variations in the types of DNA alterations that the assays detect: whereas the SCGE assay detects DNA primary lesions that are often repairable, the CBMN-cyt test detects irreparable lesions. Several studies describing combined experiments where SCGE and CBMN-cyt assays have comparatively been performed showed that the CBMN-cyt method seems to be less sensitive than SCGE assay for assessing DNA damage potential (Goethem et al., 1997; He et al., 2000; Severin et al., 2010; Tafazoli and Volders, 1996). Our current observations agree well with this concept.
Genotoxicity assessment of some cosmetic and food additives
2014, Regulatory Toxicology and PharmacologyCitation Excerpt :Moreover, including TA100 bacterial strain increases the sensitivity of the test to the aldehydes mutagenicity (Dillon et al., 1998). Nevertheless, the micronucleus assay highlights only a little amount of DNA damage, that occurs in the interphase, and that will lead to fixed chromosome abnormalities after a passage through mitosis (Tafazoli and Volders, 1996). In this context, including the comet assay increases the sensitivity of the experimental system, because it also reveals very early damages (i.e. DNA double- and single-strand breaks, alkaline labile and transient repair sites, DNA crosslink and oxidative damage) (Collins, 2013).
Comparative study of cytotoxic and genotoxic effects induced by herbicide S-metolachlor and its commercial formulation twin pack gold<sup>®</sup> in human hepatoma (HepG2) cells
2013, Food and Chemical ToxicologyCitation Excerpt :The apparent lack of sensitivity of the MN assay to the genotoxicity of the herbicide S-metolachlor compared to the comet assay might be attributable to the generation of a particular type of damage. Comparative investigations between comet and MN assays employing several compounds have been performed previously, showing that the MN technique seems to be less sensitive than single cell gel electrophoresis assay for assessing DNA damage potential (Goethem et al., 1997; He et al., 2000; Nikoloff et al., 2012; Tafazoli and Volders, 1996). Nevertheless, it should be taken into account that the difference in the sensitivity of these two end points may be attributable to the type of S-metolachlor-induced lesions differentially estimated by these assays.
Approaches to cancer assessment in EPA's Integrated Risk Information System
2011, Toxicology and Applied PharmacologyCitation Excerpt :The evidence specific to a mutagenic mode of action for 1,2,3-trichloropropane is summarized in Table 1. The experimental support for 1,2,3-trichloropropane's mutagenic mode of carcinogenic action includes: mutagenic activity demonstrated in bacterial and mammalian cell systems treated with 1,2,3-trichloropropane and activated with an S9 fraction from chemically induced rat or hamster livers (Doherty et al., 1996; Tafazoli and Kirsch-Volders, 1996; Lag et al., 1994; NTP, 1993; Ratpan and Plaumann, 1988; von der Hude et al., 1987; Haworth et al., 1983; Stolzenberg and Hine, 1980); evidence of the direct interaction of 1,2,3-trichloropropane metabolites with DNA in vivo 4 h post-exposure (Weber and Sipes, 1990); high concentrations of DNA adducts in the tumor-forming organs of both B6C3F1 mice and F344/N rats 6 h post-exposure (La et al., 1995); identification of the primary DNA adduct, S-[1-(hydroxymethyl)-2-(N7-guanyl)ethyl]glutathione (La et al., 1995), which has an inhibitory effect on sequence-specific DNA binding by regulatory proteins (Gasparutto et al., 2005; Ezaz-Nikpay and Verdine, 1994); dose-dependent increase in DNA strand breaks in hepatocytes from F344/N rats (Weber and Sipes, 1991) and in kidney cells from male Wistar rats (Lag et al., 1991); and genotoxic effects observed in vivo in the SMART in D. melanogaster (Chroust et al., 2007) and in rats with an increase in the number of mononuclear hepatocytes with a nucleus of high ploidy and decrease in the number of binuclear cells (Belyaeva et al., 1974, 1977). While 1,2,3-trichloropropane tested positive in in vivo and in vitro assays, a number of assays for 1,2,3-trichloropropane have tested non-positive for DNA reactivity and mutagenicity.