S-(1,2-Dichlorovinyl)-?-cysteine-induced dedifferentiation and p53 gene mutations in LLC-PK1 cells: a comparative investigation with S-(2-chloroethyl)cysteine, potassium bromate, cis-platinum and styrene oxide

Richter, Hedwig; Vamvakas, Spiros

doi:10.1016/s0378-4274(98)00006-x

Cited by 6 publications

(2 citation statements)

References 43 publications

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“…In a 1994 assessment of potassium bromate and sodium bromate, the Cosmetic Ingredient Review (CIR) Expert Panel stated that these ingredients may be used in cosmetic permanent wave formulations at concentrations not to exceed 10.17%, measured as sodium bromate. 1 The Expert Panel reviewed newly available studies since that assessment, along with updated information regarding types and concentrations of use 2…”

Section: Resultsmentioning

confidence: 99%

Annual Review of Cosmetic Ingredient Safety Assessments: 2007-2010

Andersen¹

2011

Int J Toxicol

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This Annual Review of Cosmetic Ingredient Safety Assessments updates and affirms the findings of the Cosmetic Ingredient Review (CIR) Expert Panel's assessment of almost 30 compounds used in cosmetic ingredients. The review also summarizes new findings from epidemiology studies of hair dyes. The CIR Expert Panel's re-review process is intended to uncover any new data since the last safety assessment. In some cases, newly available data are largely redundant compared with the data available in the original safety assessment. In other cases, new data present new safety issues. If after considering the newly available information, the CIR Expert Panel decides to not reopen a safety assessment, this finding, along with any background material, is summarized and announced publicly. To assure that the scientific community is aware of any new information and the decision not to reopen, this Annual Review of Cosmetic Ingredient Safety Assessments is prepared. A list of reference sources is provided after each ingredient re-review summary that updates the available published literature and includes any unpublished data made available since the original safety assessment. The re-review also captures information on the industry's current practices of ingredient use, updating the data available in the earlier report. Although this material provides the opinion of the CIR Expert Panel regarding the new data described, it does not constitute a full safety review. The CIR Expert Panel has assessed the safety of over 2100 cosmetic ingredients since its inception in 1976. These safety assessments were published in the

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Section: Resultsmentioning

confidence: 99%

Annual Review of Cosmetic Ingredient Safety Assessments: 2007-2010

Andersen¹

2011

Int J Toxicol

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“…Formation of 8-oxodG is known to induce G f T transversion, and this mutation is thought to contribute to activation of oncogenes and/or inactivation of tumor suppressor genes, thereby leading to carcinogenesis (8,9). There is a report that exposure of cultured renal cells to KBrO 3 resulted in the induction of p53 gene mutation (10). Furthermore, KBrO 3 has been shown to induce DNA strand breaks and poly(ADPribosyl)ation (11) and proliferative response (12) in the kidney as tumor promoting potential.…”

Section: Introductionmentioning

confidence: 99%

Requirement of Glutathione and Cysteine in Guanine-Specific Oxidation of DNA by Carcinogenic Potassium Bromate

Murata

Bansho

Inoue

et al. 2001

Chem. Res. Toxicol.

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Potassium bromate (KBrO3), a food additive, induces renal-cell tumors in rats. KBrO3 induced 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG) formation in human leukemia cell line HL-60 as well as in its H2O2-resistant clone, HP100, suggesting no involvement of H2O2. Depletion of GSH by buthionine sulfoximine (BSO) had a little inhibitory effect on KBrO3-induced 8-oxodG formation. However, the amount of 8-oxodG was still significantly higher than that in control, suggesting that intracellular Cys can affect KBrO3 to oxidize DNA, when GSH decreased. KBrO3 caused 8-oxodG in isolated DNA in the presence of GSH (tripeptide; gamma-GluCysGly), gamma-GluCys, CysGly, or Cys. Methional completely inhibited 8-oxodG formation induced by KBrO3 plus GSH, but typical hydroxyl radical scavengers, SOD and catalase, had little or no inhibitory effects. When bromine solution (BrO(-)) was used instead of BrO3(-), similar scavenger effects were observed. Experiments with 32P-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene suggested that KBrO3 induced 8-oxodG formation at 5'-site guanine of GG and GGG sequences of double-stranded DNA in the presence of GSH and that treatment of formamidopyrimidine-DNA glycosylase led to chain cleavages at the guanine residues. ESR spin-trapping studies showed that 1:2:2:1 quartet DMPO (5,5-dimethyl-1-pyrroline N-oxide) spectrum similar to DMPO/hydroxy radical (*OH) adduct, but the signals were not inhibited by ethanol. Therefore, the signal seemed not to be due to *OH but byproduct due to oxidation of DMPO by the reactive species. The signals were suppressed by the addition of dGMP, but not by other mononucleotides, suggesting the specific reactivity with guanine. On the basis of our results and previous literature, it is speculated that reduction of KBrO3 by SH compounds in renal proximal tubular cells yields bromine oxides and bromine radicals, which are the reactive species that cause guanine oxidation, leading to renal carcinogenesis of KBrO3.

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Renal Toxicity and Carcinogenicity of Trichloroethylene: Key Results, Mechanisms, and Controversies

Brüning

Bolt

2000

Critical Reviews in Toxicology

105

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The discussion on renal carcinogenicity of trichloroethylene addresses epidemiological, mechanistic, and metabolic aspects. After trichloroethylene exposure of rats, renal cell tumors were found increased in males, and an increased incidence of interstitial cell tumors of the testes was reported. Studies on the metabolism of trichloroethylene in rodents and in humans support the role of bioactivation reactions for the development of tumors following exposure to trichloroethylene. Epidemiological cohort studies addressing the carcinogenicity of trichloroethylene with respect to the renal or urothelial target sites have been conducted, and no clear evidence for an elevated renal or urinary tract cancer risk in trichloroethylene-exposed groups was visible in exposed populations. However, a cohort study of 169 male workers having been exposed to unusually high levels of trichloroethylene in Germany within the period between 1956 and 1975 supported a nephrocarcinogenic effect of trichloroethylene in humans. The results of this study were discussed in the literature with considerable reserve; criticism was based mainly on the choice of the study group, which had been recruited from personnel of a company in which a cluster of four renal tumors was observed previously. Hence, a further case-control study was conducted in the same region. This study confirmed the results of the previous cohort study, supporting the concept of involvement of prolonged and high-dose trichloroethylene exposures in the development of renal cell cancer. Further investigations on patients with renal cell carcinoma and with histories of high trichloroethylene exposures, on the basis of excretion of marker proteins in the urine, pointed to toxic damage to the proximal renal tubules by trichloroethylene. The hypothesis of implication of a glutathione transferase-dependent bioactivating pathway of trichloroethylene, established in experimental animals, seems at least also plausible for humans. Apparently, the occurrence of renal cell carcinomas in man follows high-dose exposures to trichloroethylene that are also accompanied by damage to tubular renal cells. Development of renal cell carcinomas has been related to mutations in the vonHippel-Lindau (VHL) tumor suppressor gene. Renal cell carcinoma tissues of persons with histories of prolonged high-dose exposure to trichloroethylene were investigated for the occurrence of mutations of the vonHippel-Lindau (VHL) tumor suppressor gene. VHL gene mutations were found in the majority of renal cell tumors associated with high-level exposure to trichloroethylene. A specific mutational hot spot at the VHL nucleotide 454 was addressed as a unique mutation pattern of the VHL tumor suppressor gene. A synopsis of all experimental, clinical, and epidemiological data suggests that reactive metabolites of trichloroethylene, with likely involvement of dichlorovinyl-cysteine (DCVC), exert a genotoxic effect on the proximal tubule of the human kidney. This constitutes a tumor-initiating process of genotoxic nature, ...

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S-(1,2-Dichlorovinyl)-?-cysteine-induced dedifferentiation and p53 gene mutations in LLC-PK1 cells: a comparative investigation with S-(2-chloroethyl)cysteine, potassium bromate, cis-platinum and styrene oxide

Cited by 6 publications

References 43 publications

Annual Review of Cosmetic Ingredient Safety Assessments: 2007-2010

Annual Review of Cosmetic Ingredient Safety Assessments: 2007-2010

Requirement of Glutathione and Cysteine in Guanine-Specific Oxidation of DNA by Carcinogenic Potassium Bromate

Renal Toxicity and Carcinogenicity of Trichloroethylene: Key Results, Mechanisms, and Controversies

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