Assessment of aniline derivatives-induced DNA damage in the liver cells of B6C3F1 mice using the alkaline single cell gel electrophoresis (?comet?) assay

Przybojewska, Barbara

doi:10.1002/(sici)1520-6866(1999)19:5<323::aid-tcm2>3.0.co;2-c

Cited by 6 publications

(7 citation statements)

References 10 publications

(11 reference statements)

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“…2,4,6-trimethylaniline produced mouse liver DNA strand breaks in the single cell gel electrophoresis assay (Przybojewska, 1999), but was not mutagenic and TOXICOLOGIC PATHOLOGY evidence for its carcinogenic activity was considered not evaluable by IARC (International Agency for Research on Cancer, 1982a). A structural analog, 2,4,5-trimethylaniline, has limited evidence for carcinogenicity in rodents, and was weakly mutagenic to Salmonella with bioactivation (Kugler-Steigmeier et al, 1989).…”

Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 99%

“…This probably reflects the greater susceptibility of rats to aromatic amine-induced methemoglobinemia (Kiese, 1966), which leads to splenic congestion and necrosis due to the culling of abnormal erythrocytes. In in vitro genotoxicity assays, aniline was negative (Williams et al, 1989;Przybojewska, 1999). Several related monocyclic aromatic amines have also been tested.…”

Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 99%

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Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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Toxicity and carcinogenicity in the mucosa of the nasal passages in rodents has been produced by a variety of organic chemicals which are systemically distributed. In this review, 14 such chemicals or classes were identified that produced rodent nasal cytotoxicity, but not carcinogenicity, and 11 were identified that produced nasal carcinogenicity. Most chemicals that affect the nasal mucosa were either concentrated in that tissue or readily activated there, or both. All chemicals with effects in the nasal mucosa that were DNA-reactive, were also carcinogenic, if adequately tested. None of the rodent nasal cytotoxins has been identified as a human systemic nasal toxin. This may reflect the lesser biotransformation activity of human nasal mucosa compared to rodent and the much lower levels of human exposures. None of the rodent carcinogens lacking DNA reactivity has been identified as a nasal carcinogen or other cancer hazard to humans. Some DNA-reactive rodent carcinogens that affect the nasal mucosa, as well as other tissues, have been associated with cancer at various sites in humans, but not the nasal cavity. Thus, findings in only the rodent nasal mucosa do not necessarily predict either a toxic or carcinogenic hazard to that tissue in humans.

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Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 99%

Section: Human Effects Of Rodent Nasal Cytotoxinsmentioning

confidence: 99%

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

2006

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“…2,5-Xylidine did not show oxidation path differences, and had similar LBE values and carcinogenicity in both species. Conversely, 2,4-xylidine, which may cause direct DNA damage [58], underwent demethylation at mouse CYP2E1 similar to 4-chloro-o-toluidine, and the carcinogenicity is similar.…”

Section: Docking Resultsmentioning

confidence: 99%

A combination of 3D-QSAR, docking, local-binding energy (LBE) and GRID study of the species differences in the carcinogenicity of benzene derivatives chemicals

Fratev

Benfenati

2008

Journal of Molecular Graphics and Modelling

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“…Phthalate compounds, including dibutyl phthalate, diisobutyl phthalate, bis (2-ethylhexyl) phthalate, and mono-2-ethylhexyl phthalate, have potential mutagenic and carcinogenic effects on organisms and trick a possible pathway of tumor initiation in animals [57][58][59][60][61]. Aniline is nonmutagenic [62][63][64], but its derivates such as 2,4-dimethylaniline and 2,4,6-trimethylaniline were identified as mutagens and carcinogens [65]. Aniline may react with norharman to form a mutagen (aminophenylnorharman) in organisms or in the presence of activation systems (S9 mix), which consequently causes genotoxicity [65][66][67].…”

Section: Discussionmentioning

confidence: 99%

“…Aniline is nonmutagenic [62][63][64], but its derivates such as 2,4-dimethylaniline and 2,4,6-trimethylaniline were identified as mutagens and carcinogens [65]. Aniline may react with norharman to form a mutagen (aminophenylnorharman) in organisms or in the presence of activation systems (S9 mix), which consequently causes genotoxicity [65][66][67]. Therefore, apart from the detected PAHs, other genotoxic compounds in the effluents led to the observed in vitro effects.…”

Section: Discussionmentioning

confidence: 99%

Assessment of hormonal activities and genotoxicity of industrial effluents using in vitro bioassays combined with chemical analysis

Fang

Ying

Zhao

et al. 2012

Enviro Toxic and Chemistry

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Wastewaters from various industries are a main source of the contaminants in aquatic environments. The authors evaluated the hormonal activities (estrogenic/anti‐estrogenic activities, androgenic/anti‐androgenic activities) and genotoxicity of various effluents from textile and dyeing plants, electronic and electroplate factories, pulp and paper mills, fine chemical factories, and municipal wastewater treatment plants in the Pearl River Delta region by using in vitro bioassays (yeast estrogen screen [YES]; yeast androgen screen [YAS]; and genotoxicity assay [umu/SOS]) combined with chemical analysis. The results demonstrated the presence of estrogenic, anti‐estrogenic, and anti‐androgenic activity in most industrial effluents, whereas no androgenic activities were detected in all of the effluents. The measured estrogenic activities expressed as estradiol equivalent concentrations (EEQs) ranged from below detection (3 of 26 samples) to 40.7 ng/L, with a mean of 7.33 ng/L in all effluents. A good linear relationship was found between the EEQs measured by YES bioassay and the EEQs calculated from chemical concentrations. These detected estrogenic compounds, such as 4‐nonylphenol and estrone, were responsible for the estrogenic activities in the effluents. The genotoxic effects expressed as benzo[a]pyrene equivalent concentrations (BaP EQs) varied between below detection and 88.2 µg/L, with a mean of 8.76 µg/L in all effluents. The target polycyclic aromatic hydrocarbons were minor contributors to the genotoxicity in the effluents, and some nontarget compounds in the effluents were responsible for the measured genotoxicity. In terms of estrogenic activities and genotoxicity, discharge of these effluents could pose high risks to aquatic organisms in the receiving environments. Environ. Toxicol. Chem. 2012;31:1273–1282. © 2012 SETAC

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Assessment of aniline derivatives-induced DNA damage in the liver cells of B6C3F1 mice using the alkaline single cell gel electrophoresis (?comet?) assay

Cited by 6 publications

References 10 publications

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

Nasal Cytotoxic and Carcinogenic Activities of Systemically Distributed Organic Chemicals

A combination of 3D-QSAR, docking, local-binding energy (LBE) and GRID study of the species differences in the carcinogenicity of benzene derivatives chemicals

Assessment of hormonal activities and genotoxicity of industrial effluents using in vitro bioassays combined with chemical analysis

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