Reproducibility of microbial mutagenicity assays: I. Tests withSalmonella typhimurium andEscherichia coli using a standardized protocol

Dunkel, Virginia C.; Zeiger, Errol; Brusick, David; McCoy, Elena C.; McGregor, Douglas; Mortelmans, Kristien; Rosenkranz, Herbert S.; Simmon, Vincent F.

doi:10.1002/em.2860060702

Cited by 154 publications

(16 citation statements)

References 7 publications

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“…To address this issue, a set of international, collaborative testing programs was established to evaluate the Salmonella assay as well as several other mutagenicity assays using coded chemicals from the same lot (Ashby et al 1985, 1988; de Serres et al 1981) and standard protocols (Dunkel et al 1984, 1985; Margolin et al 1984; Piegorsch and Zeiger 1991). These comparative studies paved the way for the establishment of standard methods and procedures for selected mutagenicity assays that are still largely in place.…”

Section: The Salmonella Assay As a Model For 21st Century Toxicology mentioning

confidence: 99%

TheSalmonellaMutagenicity Assay: The Stethoscope of Genetic Toxicology for the 21st Century

Claxton

Umbuzeiro

DeMarini

2010

Environ Health Perspect

133

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ObjectivesAccording to the 2007 National Research Council report Toxicology for the Twenty-First Century, modern methods (e.g., “omics,” in vitro assays, high-throughput testing, computational methods) will lead to the emergence of a new approach to toxicology. The Salmonella mammalian microsome mutagenicity assay has been central to the field of genetic toxicology since the 1970s. Here we document the paradigm shifts engendered by the assay, the validation and applications of the assay, and how the assay is a model for future in vitro toxicology assays.Data sourcesWe searched PubMed, Scopus, and Web of Knowledge using key words relevant to the Salmonella assay and additional genotoxicity assays.Data extractionWe merged the citations, removing duplicates, and categorized the papers by year and topic.Data synthesisThe Salmonella assay led to two paradigm shifts: that some carcinogens were mutagens and that some environmental samples (e.g., air, water, soil, food, combustion emissions) were mutagenic. Although there are > 10,000 publications on the Salmonella assay, covering tens of thousands of agents, data on even more agents probably exist in unpublished form, largely as proprietary studies by industry. The Salmonella assay is a model for the development of 21st century in vitro toxicology assays in terms of the establishment of standard procedures, ability to test various agents, transferability across laboratories, validation and testing, and structure–activity analysis.ConclusionsSimilar to a stethoscope as a first-line, inexpensive tool in medicine, the Salmonella assay can serve a similar, indispensable role in the foreseeable future of 21st century toxicology.

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Section: The Salmonella Assay As a Model For 21st Century Toxicology mentioning

confidence: 99%

TheSalmonellaMutagenicity Assay: The Stethoscope of Genetic Toxicology for the 21st Century

Claxton

Umbuzeiro

DeMarini

2010

Environ Health Perspect

133

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“…Although lead toxicity on different biological systems and functions has been well reported (2)(3)(4), there are conflicting data on its genotoxic and carcinogenic properties. In bacterial tests, lead seems to be generally nonmutagenic (5). Nevertheless, in eukaryotic cells this metal is usually genotoxic (6,7), through a mechanism that until now has not been well characterized and that possibly involves indirect damage to DNA, affecting the stabilization of chromatin (8) or interacting with repair processes (9).…”

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Occupational exposure to lead and induction of genetic damage.

Vaglenov

Creus

Laltchev

et al. 2001

Environ Health Perspect

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To investigate whether occupational exposure to lead is genotoxic, we evaluated data from 103 lead-exposed workers and 78 matched controls. These data correspond to three different sampling periods, and we measured genetic damage as increases in the frequency of binucleated cells with micronuclei (BNMN) in peripheral blood lymphocytes. The levels of exposure were determined according to the lead levels in blood. Clearly significant increases in BNMN were observed in the exposed groups when compared to the control group. In addition, for the overall population (n = 181), we observed a clear relationship between lead levels in blood and BNMN (r = 0.497; p < 0.001). When we examined four exposure levels--very low exposure (< 1.20 microM/L), low exposure (1.20-1.91 microM/L), high exposure (1.92-2.88 microM/L), and very high exposure (> 2.88 microM/L)--we found significant differences in the genetic damage induction. We conclude that exposure to levels of lead higher than 1.20 microM/L may pose an increase in genetic risk. In addition, our data show that blood lead level is a good indicator of genetic damage induction.

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“…In bacterial tests, lead seems to be generally nonmutagenic (5). Nevertheless, in eukaryotic cells this metal is usually genotoxic (6,7), through a mechanism that until now has not been well characterized and that possibly involves indirect damage to DNA, affecting the stabilization of chromatin (8) or interacting with repair processes (9).…”

Section: Lead (Pb) a Toxic Contaminant Metal Used In Many Important mentioning

confidence: 99%

Occupational Exposure to Lead and Induction of Genetic Damage

Vaglenov¹,

Creus²,

Laltchev³

et al. 2001

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.To investigate whether occupational exposure to lead is genotoxic, we evaluated data from 103 lead-exposed workers and 78 matched controls. These data correspond to three different sampling periods, and we measured genetic damage as increases in the frequency of binucleated cells with micronuclei (BNMN) in peripheral blood lymphocytes. The levels of exposure were determined according to the lead levels in blood. Clearly significant increases in BNMN were observed in the exposed groups when compared to the control group. In addition, for the overall population (n = 181), we observed a clear relationship between lead levels in blood and BNMN (r = 0.497; p < 0.001). When we examined four exposure levels-very low exposure (< 1.20 piM/L), low exposure (1.20-1.91 pM/L), high exposure (1.92-2.88 pM/L), and very high exposure (> 2.88 pM/L)-we found significant differences in the genetic damage induction. We conclude that exposure to levels of lead higher than 1.20 pM/L may pose an increase in genetic risk. In addition, our data show that blood lead level is a good indicator of genetic damage induction. This investigation was supported in part by the Bulgarian government (HZ-13/92) and by a contract with Elhim-Izkra Ltd. (N97/21.03.1996). We thank N. Bandev, director of the starter battery plant, for his financial support. We are grateful to the Spanish Ministry of Education and Culture, which granted a visiting research position to A. Vaglenov (DGES, SAB 1995-0689). We are indebted to G. Umbert and A. Corral for their expert technical assistance. The secretarial help of M. McCarthy is very much appreciated.

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Reproducibility of microbial mutagenicity assays: I. Tests withSalmonella typhimurium andEscherichia coli using a standardized protocol

Cited by 154 publications

References 7 publications

TheSalmonellaMutagenicity Assay: The Stethoscope of Genetic Toxicology for the 21st Century

TheSalmonellaMutagenicity Assay: The Stethoscope of Genetic Toxicology for the 21st Century

Occupational exposure to lead and induction of genetic damage.

Occupational Exposure to Lead and Induction of Genetic Damage

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