Failure of chloroform to induce chromosome damage or sister-chromatid exchanges in cultured human lymphocytes and failure to induce reversion in Escherichia coli

Kirkland, David; Smith, Katie; Abbé, N.J. Van

doi:10.1016/0015-6264(81)90517-4

Cited by 27 publications

(8 citation statements)

References 8 publications

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“…Several reports indicate that carbon tetrachloride is not mutagenic in S. typhimurium tester strains using either the pourplate or preincubation method Uehleke et al, 1977;Zeiger et al, 1988]; chloroform also is negative in S. typhimurium and E. coli tester strains using these testing protocols [Simmon et al, 1977;Uehleke et al, 1977;Gocke et al, 1981;Kirkland et al, 1981;Van Abbe et al, 1982]. We previously performed a literature review which indicated that some poorly water-soluble, volatile compounds such as 1-bromopropane (boiling point, 71°C) and 1-bromobutane (boiling point 102°C) give negative bacterial mutagenicity responses when using the pour-plate or preincubation methods, but have produced positive response when a gas exposure method is employed [Araki et.…”

Section: Introductionmentioning

confidence: 97%

Mutagenicity of carbon tetrachloride and chloroform in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, using a gas exposure method

Araki

Kamigaito

Sasaki

et al. 2004

Environ and Mol Mutagen

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The volatile solvents carbon tetrachloride and chloroform are carcinogens that are often reported as nonmutagenic in bacterial mutagenicity assays. In this study, we evaluated the mutagenicity of these compounds in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, with and without S9 mix, using a gas exposure method. Tests were also conducted with a glutathione-supplemented S9 mix. Carbon tetrachloride was mutagenic in TA98 without S9 mix, and in WP2/pKM101 and WP2uvrA/pKM101 with and without S9 mix; carbon tetrachloride was not mutagenic in TA100, TA1535 or TA1537. Chloroform was mutagenic in WP2/pKM101, but only in the presence of glutathione-supplemented S9 mix. Chloroform was not mutagenic in TA98, TA100, TA1535, TA1537, or WP2uvrA/pKM101 with or without S9 mix, and was not mutagenic in TA98, TA100, TA1535, TA1537, or WP2uvrA/pKM101 in the presence of glutathione-supplemented S9 mix. The data indicate that carbon tetrachloride and chloroform are bacterial mutagens when adequate exposure conditions are employed and suggest that a genotoxic mode of action could contribute to the carcinogenicity of these compounds.

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Section: Introductionmentioning

confidence: 97%

Mutagenicity of carbon tetrachloride and chloroform in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, using a gas exposure method

Araki

Kamigaito

Sasaki

et al. 2004

Environ and Mol Mutagen

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“…Chloroform administered in corn oil has been shown to induce hepatocellular carcinomas in mice and epithelial tumors in the kidney of male rats (35). The inability of chloroform to bind significantly to liver and kidney DNA (44)(45)(46) and its lack or very low level of genotoxicity (31,(36)(37)(38)(39)(40)(41)(42)(43) has led to the proposal that the carcinogenicity of chloroform results from a nongenotoxic mechanism such as tumor promotion (45,46). Because the mechanism of carcinogenicity (i.e., genotoxic or nongenotoxic) of a substance has major implications in interspecies and low-dose extrapolation, we attempted to demonstrate the nongenotoxic and tumor-promoting mechanism for the carcinogenic activity of chloroform.…”

Section: Resultsmentioning

confidence: 99%

“…The administration of chloroform in corn oil by gavage induced liver tumors in B6C3F1 mice (35). Chloroform has been shown to lack or at most possess minimum genotoxic activity (31,(36)(37)(38)(39)(40)(41)(42) and has also been shown to not bind significantly to liver or kidney DNA in rats (43)(44)(45). These findings have led to the proposal that the hepatocarcinogenicity of chloroform in mice results from a nongenotoxic mechanism such as tumor promotion (45,46).…”

Section: Introductionmentioning

confidence: 98%

Carcinogenicity of by-products of disinfection in mouse and rat liver.

Herren-Freund¹,

Pereira²

1986

Environ Health Perspect

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By-products of disinfection were tested for initiating and/or promoting activity in rat liver by using the rat liver foci bioassay. The assay uses an increased incidence of -y-glutamyltranspeptidase-positive foci (GGT foci) as an indicator of carcinogenicity. The by-products of disinfection, including chloramine, halogenated humic acids, halogenated ethanes, halogenated acetonitriles, halogenated methanes, halogenated ethylenes, and N-Cl-piperidine, did not initiate GGT foci, which would indicate that they are not capable of initiating carcinogenesis. Chloroform and halogenated benzenes were tested in this assay for their ability to promote the occurrence of GGT foci and tumors initiated by diethylnitrosamine (DENA). Chloroform (1800 ppm in the drinking water) either had no effect or inhibited the occurrence of GGT foci when administered subsequent to a single dose of DENA. However, when the chloroform was administered in drinking water concurrently with weekly doses of DENA, it enhanced the formation of liver tumors. Of 20 halogenated benzenes tested, only 1,2,4,5-tetrachlorobenzene and hexachlorobenzene promoted the occurrence of DENA-initiated GGT foci. Thus in rat liver, the tested by-products of drinking water disinfection did not demonstrate tumor-initiating activity, although a few appeared to possess tumor-promoting activity.Chloroform was also tested for tumor-promoting activity in 15-day-old Swiss mice initiated with ethylnitrosourea (ENU). At weaning they started to receive either 1800 ppm chloroform or 500 ppm sodium phenobarbital (the positive control for tumor promotion) in their drinking water. The mice continued to receive either chloroform or phenobarbital until 51 weeks of age and were sacrificed at 52 weeks of age. ENU at 5 and 20 ,ug/g caused a dose-dependent increase in liver tumors. In male mice, chloroform inhibited both spontaneous and ENU-induced liver tumors. When administered in the drinking water, chloroform inhibited, whereas phenobarbital promoted, hepatocarcinogenesis in mice.

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“…3,4 mM) keine Induktion von SCE nachgewiesen (k. A. über Inkubationsbedingungen; Kirkland et al 1981), ab 10 mM Chloroform wurde ein Anstieg an SCE pro Zelle um den Faktor 1,2-1,8 beobachtet (k. A. über Inkubationsbedingungen; Morimoto und Koizumi 1983). In K 3 DZellen ("permanent leukemia cell line, Long-Evans rats") stieg bei 1 mM die SCEHäufigkeit in Anwesenheit eines metabolischen Aktivierungssystems (S9 aus PCBinduzierter Rattenleber) signifikant auf 10,0 SCE pro Zelle an, in Abwesenheit eines metabolischen Aktivierungssystems war das Ergebnis mit 7,4 SCE nach Aussagen der Autoren negativ (k. A. über Inkubationsbedingungen; Fujie et al 1993).…”

Section: Indikatortestsunclassified

“…3,4 mM) negativ (Kirkland et al 1981). Angaben zur Zytotoxizität sowie zur Durchführung der Inkubation werden nicht gemacht.…”

Section: Zytogenetische Testsunclassified

Chloroform (Trichlormethan) [MAK Value Documentation in German language, 2003]

2012

The MAK‐Collection for Occupational Health and Safety

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Failure of chloroform to induce chromosome damage or sister-chromatid exchanges in cultured human lymphocytes and failure to induce reversion in Escherichia coli

Cited by 27 publications

References 8 publications

Mutagenicity of carbon tetrachloride and chloroform in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, using a gas exposure method

Mutagenicity of carbon tetrachloride and chloroform in Salmonella typhimurium TA98, TA100, TA1535, and TA1537, and Escherichia coli WP2uvrA/pKM101 and WP2/pKM101, using a gas exposure method

Carcinogenicity of by-products of disinfection in mouse and rat liver.

Chloroform (Trichlormethan) [MAK Value Documentation in German language, 2003]

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