Primary DNA damage in chrome-plating workers

Gambelunghe, Angela; Piccinini, R.; Ambrogi, Maura; Villarini, Milena; Moretti, Massimo; Marchetti, Cristina; Abbritti, Giuseppe; Muzi, Giacomo

doi:10.1016/s0300-483x(03)00088-x

Cited by 87 publications

(46 citation statements)

References 37 publications

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“…Likewise, the findings of Danadevi et al [2001], who investigated the genotoxic effects of K 2 CrO 4 , on Swiss albino male mice, support the findings by Gambelunghe et al [2003] of increased DNA damage in Cr-exposed workers. The data of Danadevi et al [2001] are noteworthy, because they illustrate how early and at what low doses direct DNA damage can occur.…”

Section: Oxidative Damagesupporting

confidence: 73%

“…This finding led the authors to conclude that the detection of apoptosis may have been hindered by the very low Cr body burden in the chrome-plating workers in this study. Although apoptosis was not demonstrated by Gambelunghe et al [2003], in this in vivo human study, primary DNA damage was seen in peripheral lymphocytes and several authors have reported that Cr (VI) induces apoptosis in mammalian and human cell lines. For example, apoptosis was found in the murine keratinocytes, Pam 212-ras cells at the IC50 of 76 lM [Flores and Perez, 1999], in CHO cells , and in the human lung epithelial cell line, A546 at concentrations ranging from 75 to 300 lM [Ye et al, 1999].…”

Section: Oxidative Damagementioning

confidence: 75%

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An evaluation of the mode of action framework for mutagenic carcinogens case study II: Chromium (VI)

McCarroll

Keshava

Chen

et al. 2009

Environ and Mol Mutagen

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In response to the 2005 revised U.S Environmental Protection Agency's (EPA) Cancer Guidelines, a strategy is being developed to include all mutagenicity and other genotoxicity data with additional information to determine whether the initiating step in carcinogenesis is through a mutagenic mode of action (MOA). This information is necessary to decide if age-dependent adjustment factors (ADAFs) should be applied to the risk assessment. Chromium (VI) [Cr (VI)], a carcinogen in animals and humans via inhalation, was reassessed by the National Toxicology Program (NTP) in 2-year drinking water studies in rodents. From these data, NTP concluded that the results with Cr (VI) showed clear evidence of carcinogenicity in male and female mice and rats. Cr (VI) is also mutagenic, in numerous in vitro assays, in animals (mice and rats) and in humans. Accordingly, Cr (VI) was processed through the MOA framework; postulated key steps in tumor formation were interaction of DNA with Cr (VI) and reduction to Cr (III), mutagenesis, cell proliferation, and tumor formation. Within the timeframe and tumorigenic dose range for early events, genetic changes in mice (single/double-stranded DNA breaks) commence within 24 hr. Mechanistic evidence was also found for oxidative damage and DNA adduct formation contributing to the tumor response. The weight of evidence supports the plausibility that Cr (VI) may act through a mutagenic MOA. Therefore, the Cancer Guidelines recommend a linear extrapolation for the oral risk assessment. Cr (VI) also induces germ cell mutagenicity and causes DNA deletions in developing embryos; thus, it is recommended that the ADAFs be applied.

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Section: Oxidative Damagesupporting

confidence: 73%

Section: Oxidative Damagementioning

confidence: 75%

An evaluation of the mode of action framework for mutagenic carcinogens case study II: Chromium (VI)

McCarroll

Keshava

Chen

et al. 2009

Environ and Mol Mutagen

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“…It is basically used in chrome plating and thus poses a serious occupational hazard. DNA damage in chrome plating workers of Italy was studied by Gambelunghe et al [92]. They estimated DNA strand breaks of single cell microgel electrophoresis and apoptosis by flow cytometry after propidium iodide staining of the cells.…”

Section: Apoptosismentioning

confidence: 99%

Metals and apoptosis: Recent developments

Rana

2008

Journal of Trace Elements in Medicine and Biology

326

175

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“…In sodium chromate Cr-51 injections, chromium is present as a hexavalent, which is the most potent carcinogen of the various groups of chromium compounds tested. Hexavalent chromium inhibits DNA synthesis (Bridgewater et al 1998;Gambelunghe et al 2003;Bagchi et al 2002) and cause DNA damage, as has strong aYnity to nucleic acid and may be involved in maintaining of the nucleic acid tertiary structure (Mertz 1986;McLean 1983). A signiWcantly reduced number of viable fetuses implantation sites has been reported in mice exposed to hexavalent chromium (Elbetieha and Al-Hamood 1997).…”

Section: Discussionmentioning

confidence: 96%