Induction of chromosomal aberrations in cultured Chinese hamster cells by short-term treatment with cadmium chloride

Ochi, Takafumi; Mogi, Masayuki; Watanabe, Mitsuo; Ohsawa, Motoyasu

doi:10.1016/0165-1218(84)90098-3

Cited by 38 publications

(9 citation statements)

References 19 publications

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“…Cadmium is known to induce structural and numerical chromosome aberrations in other species and there is considerable evidence for its clastogenicity. It has been shown to induce DNA strand-breakage, chromosomal aberrations and sister chromatid exchanges in various mammalian cells in vitro (Ochi et al, 1984;Howard et al, 1991;Coogan et al, 1992); but at much higher levels (> 1 mg L -1 ) than the ones we tested in vivo.…”

Section: Aneuploidymentioning

confidence: 60%

Effects of cadmium on aneuploidy and hemocyte parameters in the Pacific oyster, Crassostrea gigas

et al. 2006

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Pacific oysters, Crassostrea gigas, are commonly reared in estuaries where they are exposed to anthropogenic pollution. Much research has been made on the toxicity of cadmium to aquatic organisms because the compound recurrently contaminates their environment. Our study examined the influence of cadmium on aneuploidy level (lowered chromosome number in a percentage of somatic cells) and hemocyte parameters in C. gigas at different stages of life. Adults and juveniles were exposed to two different concentrations of cadmium. The first concentration applied was equivalent to a peak value found in Marennes-Oléron bay (Charente-Maritime, France; 50 ngL(-1)) and the second was 10 times higher (500 ngL(-1)). Exposure to 50 ngL(-1) cadmium caused a significant decrease in the survival time of C. gigas, but exposure to 500 ngL(-1) surprisingly affected the survival time positively. Significant differences in aneuploidy level were observed between the cadmium treatments and the control in adults but not in juveniles or the offspring of the adult groups. The effects of cadmium on hemocyte parameters were analyzed by flow cytometry. Several hemocyte parameters increased significantly after 21 days of cadmium exposure and subsequently decreased. Phenoloxidase-like activity, evaluated by spectrophotometry, varied over the time of the experiment and increased after 66 days of contact with 500 ngL(-1) cadmium. Taken together, cadmium at environmentally relevant concentrations seems to have only moderate effects on aneuploidy and hemocyte parameters.

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Section: Aneuploidymentioning

confidence: 60%

Effects of cadmium on aneuploidy and hemocyte parameters in the Pacific oyster, Crassostrea gigas

et al. 2006

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“…Cd is a ubiquitous environmental contaminant that induces cytotoxicity, chromosomal aberrations, DNA strand breakage, and mutagenicity in mammalian cells ( − ). A significant body of evidence confirms Cd carcinogenicity in animal models; e.g., Cd has been shown to induce tumors in testes, lungs, prostates, hematopoietic systems, and at injection sites ( , ).…”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species May Participate in the Mutagenicity and Mutational Spectrum of Cadmium in Chinese Hamster Ovary-K1 Cells

Jia

Lin

1996

Chem. Res. Toxicol.

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The molecular nature of mutations induced by Cd was investigated in this study to elucidate the role of Cd in the initiation of carcinogenesis. Exposing Chinese hamster ovary (CHO)-K1 cells to cadmium acetate markedly decreased the colony-forming ability of cells and induced mutation frequency in the hypoxanthine (guanine) phosphoribosyltransferase (hprt) gene. The mutation frequency induced by Cd at LD30-LD20 doses was approximately 20 times that of untreated cells. D-Mannitol, a scavenger of reactive oxygen species (ROS), significantly protects cells against Cd cytotoxicity and mutagenicity. Furthermore, non-cytotoxic doses of 3-amino-1,2,4-triazole, a catalase inhibitor, potentiates Cd cytotoxicity and mutagenicity. The cellular Cd uptake ability was not altered by the combined treatment with either D-mannitol or 3-amino-1,2,4-triazole. The GSH level and the activities of GSH peroxidase, GSSG reductase, and catalase in cells treated with Cd (4 microM, 4 h) decreased to 78%, 47%, 40%, and 22% of the untreated cells, respectively. Those enzymatic activities recovered to normal levels 8 h after removing Cd. Polymerase chain reaction and DNA sequencing analysis of 54 independent Cd mutants revealed Cd-induced base substitutions, splice mutations, and large genomic deletions. All six types of base substitutions were observed; however, base transversions (22/27; 81%) occurred more frequently than transitions (5/27; 19%). The frequencies of mutations occurring at T.A or G.C base pairs were roughly equal. Results in this study strongly suggest that Cd mutagenicity in CHO-K1 cells is ROS-dependent. Moreover, the unique mutational spectrum induced by Cd implies that specific DNA adducts generated through the interaction of Cd-DNA and ROS may play a role in the mutational specificity.

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“…However, this may be due to a reduction of bioavailability of cadmium(II) by interaction with media components (24). In V79 Chinese hamster cells, CdCl2 induced DNA single-strand breaks, DNA-protein cross-links (25), and chromosomal aberrations (26). Furthermore, it enhanced the number of mutations at the thymidine kinase (tk) locus in mouse lymphoma L51784/TK+-cells (27) and at the hprt locus in V79 cells (25,28 Table 2.…”

Section: Cadmium(ii)mentioning

confidence: 99%

Role of DNA Repair Inhibition in Lead- and Cadmium-Induced Genotoxicity: A Review

Hartwig¹

1994

Environmental Health Perspectives

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Compounds of lead and cadmium have been shown to be carcinogenic to humans and experimental animals. However, the underlying mechanisms are still not understood. In mammalian cells in culture, lead(lIl) is weakly mutagenic after long incubation times and generates DNA strand breaks only after treatment with high, toxic doses. Cadmium(ll) induces DNA strand breaks and chromosomal aberrations, but its mutagenic potential is rather weak. However, both metals exert pronounced indirect genotoxic effects. Lead(ll) is comutagenic towards UV and N-methyl-N-nitro-Nnitrosoguanidine (MNNG) and enhances the number of UV-induced sister chromatid exchanges in V79 Chinese hamster cells. With regard to DNA repair, lead(ll) causes an accumulation of DNA strand breaks after UV-irradiation in HeLa cells, indicating an interference with the polymerization or ligation step in excision repair. Cadmium(ll) enhances the mutagenicity of UV light in V79 Chinese hamster cells and an increased sensitivity toward UV light is observed in various rodent and human cell lines. Furthermore, an inhibition of unscheduled DNA synthesis after UV-irradiation and a partial inhibition of the removal of UV-induced DNA lesions has been shown. For both metals, the indirect genotoxic effects are observed at low, nontoxic concentrations, suggesting that an interference with DNA repair processes may be predominant at biologically relevant concentrations. This might also explain the conflicting results of epidemiological studies obtained for both metals. Possible mechanisms of repair inhibiton are discussed.-Environ Health Perspect 102(Suppl 3): 45-50 (1994).

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Induction of chromosomal aberrations in cultured Chinese hamster cells by short-term treatment with cadmium chloride

Cited by 38 publications

References 19 publications

Effects of cadmium on aneuploidy and hemocyte parameters in the Pacific oyster, Crassostrea gigas

Effects of cadmium on aneuploidy and hemocyte parameters in the Pacific oyster, Crassostrea gigas

Reactive Oxygen Species May Participate in the Mutagenicity and Mutational Spectrum of Cadmium in Chinese Hamster Ovary-K1 Cells

Role of DNA Repair Inhibition in Lead- and Cadmium-Induced Genotoxicity: A Review

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