Metal Mutagenesis

Rossman, Toby G.

doi:10.1007/978-3-642-79162-8_17

Cited by 21 publications

(8 citation statements)

References 182 publications

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“…The higher genotoxicity of Cr(VI) than Cr(III) determined in our experiments has also been described by Němeček et al (2002). Rossman (1995) mentioned that the molecular mechanism of DNA damage by Cr(VI) involves the induction of DNA-DNA and DNA-protein cross-links. Furthermore, the genotoxic effect can also be increased by reactive oxygen produced during intracellular reduction.…”

Section: Genotoxicity Studysupporting

confidence: 49%

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Plants as models for chromium and nickel risk assessment

Fargašová

2012

Ecotoxicology

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The adverse effects of Cr(III), Cr(VI), and Ni(II) expressed as root and shoot growth inhibition, metal accumulation and translocation throughout plants, and genotoxicity study were examined. To examine phytoxicity and metal accumulation, Vicia sativa, Raphanus sativus, Zea mays and Sinapis alba plants were used. Except for S. alba root growth inhibition, Ni had the strongest inhibitory effect on root and shoot growth. The inhibitory rank order based on IC₅₀ values was Ni(II) > Cr(VI) > Cr(III). Z. mays was the least sensitive to all metals. While the accumulation of Cr was higher in the roots than the upper plant parts, Ni transport to shoots was at least two times higher than that of Cr. The highest accumulation of Cr was found in Z. mays and that of Ni in V. sativa and Z. mays roots. For all plants, the translocation factor was higher for Cr(VI) than for Cr(III). The translocation factor for Ni was several times higher than those of Cr. For mutagenicity assay, root tips of V. sativa, R. sativus and Z. mays were used. All metals exerted a significant increase of chromosomal aberrations and the rank order of aberrations was: Cr(VI) > Ni(II) > Cr(III). Genotoxic effects of metals were also determined by analysis of micronuclei frequency in the pollen tetrads of Tradescantia plants. None of metals significantly stimulated micronuclei frequency and the genotoxic effect decreased in the following order: Cr(VI) ≥ Ni(II) > Cr(III).

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Section: Genotoxicity Studysupporting

confidence: 49%

“…Furthermore, the genotoxic effect can also be increased by reactive oxygen produced during intracellular reduction. Rossman (1995) and Patierno and Costa (1987) found that mutations after Ni applications can result from DNA damage and DNA-protein cross-links formation.…”

Section: Genotoxicity Studymentioning

confidence: 97%

Plants as models for chromium and nickel risk assessment

Fargašová

2012

Ecotoxicology

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“…The co-mutagenic effect plays an important role in the pathogenecity of arsenic. When in combination with other metals, alkylating compounds or UV radiation, all of which are mutagens, arsenic can initiate tumour development at lower concentrations than are normally necessary to trigger the neoplastic process [1,2]. The epidemiological data on the potential carcinogenicity of lead compounds are relatively novel, contrary to the well established hematological, neurological and nephrological effects of long-term exposure to lead.…”

Section: Introductionmentioning

confidence: 96%

“…to cadmium, lead and arsenic, an interaction of the chemicals, increasing cancer risk, should be considered. In Scandinavian studies, the standardized mortality ratio (SMR) due to lung cancer amounted to 3.6 for nonsmokers exposed to arsenic, 4.9 for smokers not exposed to arsenic and to as much as 14.6 for smokers exposed to arsenic [1,2]. The development of the neoplastic disease is usually a long-lasting process, and its first symptoms often appear relatively late.…”

Section: Introductionmentioning

confidence: 98%

The Concentration of Selected Cancer Markers (TPA, TPS, Cyfra 21-1, CEA) in Workers Occupationally Exposed to Arsenic (As) and Some Heavy Metals (Pb, Cd) During a Two-Year Observation Study

Szymańska–Chabowska

Antonowicz−Juchniewicz²,

Andrzejak³

2007

International Journal of Occupational Medicine and Environmental Health

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The strong positive correlation between blood concentrations of Cd and CEA, the marker of abnormal cellular differentiation, may reflect neoplastic transformation of normal cells stimulated by some carcinogens (e.g. cadmium). All the examined carcinogenic, or potentially carcinogenic metals (As, Cd, Pb) belong to the group of factors having impact on serum TPS and/or TPA concentrations in exposed workers. No correlation was found between CYFRA 21-1 and any metal studied but it is plausible that changes in the concentration level of this marker might be revealed after a longer observation period.

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“…Metals are known co-mutagens and increase the mutagenicity of ultraviolet light, X-rays and alkylating agents (Rossman 1995, Gebel 2001). Cotreatment of As or Cd with B [a]P decreased the DNA repair process and persistence of DNA lesions in human white blood cells and SV4O-transformed fibroblasts (Hartmann and Speit 1996).…”

Section: Genotoxicity Of Pahs and Metalsmentioning

confidence: 99%

Evaluation of interaction and combined toxicity of polyaromatic hydrocarbons (PAHs) and metals using human cell-based bioassays

Muthusamy¹

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Mixed contamination of polyaromatic hydrocarbons (PAHs) and metals are ubiquitous in the environment. Some of the individual PAHs are known as human carcinogens, and metals are associated with various systemic toxicity and cancers in humans. Although the individual toxicity of PAHs and metals are well documented, our present state of knowledge about the adverse health effects of these mixtures is very limited in terms of exposure associated toxicity in humans, the underlying mechanism of toxicity and predicting the toxicity of mixtures. Due to this, their risk assessment has been mostly carried out based on their individual toxicity data.This research work investigated the interaction and combined toxicity of four PAHs

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Metal Mutagenesis

Cited by 21 publications

References 182 publications

Plants as models for chromium and nickel risk assessment

Plants as models for chromium and nickel risk assessment

The Concentration of Selected Cancer Markers (TPA, TPS, Cyfra 21-1, CEA) in Workers Occupationally Exposed to Arsenic (As) and Some Heavy Metals (Pb, Cd) During a Two-Year Observation Study

Evaluation of interaction and combined toxicity of polyaromatic hydrocarbons (PAHs) and metals using human cell-based bioassays

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