An assessment of the genetic toxicology of antimony trioxide

Elliott, B.M.; Mackay, James; Clay, Philip; Ashby, John

doi:10.1016/s1383-5718(98)00065-5

Cited by 29 publications

(26 citation statements)

References 6 publications

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“…In vitro and in vivo experimental studies have found genotoxic (clastogenic) effects of trivalent antimony (Sb 2 O 3 and SbCl 3 ): increased frequencies of sister chromatid exchange (SCE) [Kuroda et al, 1991;Gebel et al, 1997], micronuclei induction [Huang et al, 1998;Schaumloffel and Gebel, 1998;Migliore et al, 1999], and chromosomal aberrations [Elliot et al, 1998;Gurnani et al, 1992Gurnani et al, , 1993. On the basis of sufficient evidence for carcinogenicity by inhalation in experimental animals [Groth et al, 1986;Watt, 1983], the International Agency for Research on Cancer [IARC, 1989] classified Sb 2 O 3 as a possible carcinogen to humans (Group 2B).…”

Section: Introductionmentioning

confidence: 99%

Genotoxic risk and oxidative DNA damage in workers exposed to antimony trioxide

Cavallo

Iavicoli

Setini

et al. 2002

Environ and Mol Mutagen

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The growing use of antimony (Sb) compounds in industry and the consequent increase in the number of exposed workers make it important to carry out a health risk assessment. The main goal of this study was to assess the genotoxicity of Sb(2)O(3) in occupationally exposed workers. Genotoxicity was evaluated by the sister chromatid exchange (SCE) and micronucleus tests, and the enzyme (Fpg)-modified comet assay. In addition, antimony exposure levels were established by environmental monitoring with personal air samplers. We studied 23 male workers assigned to different fire retardant treatment tasks in the car upholstery industry and a control group of 23 healthy nonexposed males. The exposed workers were divided into two groups on the basis of their tasks and the work cycle: Group A comprised finishing and intermediate inspection operators who directly handled a mixture containing Sb(2)O(3); Group B were jet operators, not directly exposed to the compound. Environmental monitoring detected low Sb exposure levels but significant differences between the two groups, with Group A having the higher exposure level. Cytogenetic analyses showed no difference between exposed workers and controls for micronuclei and SCE. The enzyme-modified comet assay showed a probable relation between moderate levels of oxidative DNA damage and exposure to antimony, with a significantly higher proportion of workers in Group A having oxidative DNA damage compared to controls. The results support the theory that oxidative DNA damage is involved in the genotoxicity of antimony and indicate the need for further research in this field.

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Section: Introductionmentioning

confidence: 99%

Genotoxic risk and oxidative DNA damage in workers exposed to antimony trioxide

Cavallo

Iavicoli

Setini

et al. 2002

Environ and Mol Mutagen

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“…Only Sb III , but not Sb V compounds cause chromosome aberrations at high concentrations in human lymphocytes [181], but high concentrations of Sb V induced MN formation in human lymphocytes. These were mostly centromere negative, indicating clastogenesis [182].…”

Section: Antimonymentioning

confidence: 86%

“…However, Elliott et al [181] did not find induction of MN in bone marrow after acute or chronic exposure of mice. To resolve this inconsistency [188], gave repeated doses (250, 500 and 1000 mg/kg) of antimony trioxide to rats by oral gavage for 14 or 21 days.…”

Section: Antimonymentioning

confidence: 94%

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Genetic Toxicology of Arsenic and Antimony

Rossman¹,

Klein²

2010

Biological Chemistry of Arsenic, Antimony and Bismuth

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Interest in the genetic toxicology of arsenic (As) is motivated by the fact that it is considered as a human carcinogen [1]. The genetic toxicology of arsenicals mainly pertains to that of the trivalent arsenical arsenite (As III ) (Chapter 8) and its trivalent monomethylated and dimethylated metabolites (MMA III and DMA III ) (Chapter 7). The corresponding pentavalent compounds are both less toxic and less genotoxic than the trivalent compounds. This is because the pentavalent compounds are less reactive than the trivalent compounds, which can enter cells more readily than the pentavlent compounds (Chapter 8). Once inside the cell, pentavalent compounds are immediately reduced to trivalent compounds, so the genetic toxicology is attributed to the trivalent species and their products. However, the thioarsenical metabolite dimethyldithioarsinic acid (DMDTA V ), which is pentavalent, shows cytotoxicity and genotoxicty that resembles DMA III rather than DMA V [2]. It must also be kept in mind that some cell lines are able to methylate arsenite. Although hepatocytes are not often used for assessing genotoxicity, rat hepatocytes have a higher rate of methylation than that of human hepatocytes [3]. Insignificant amounts or no methylation was seen in normal human keratinocytes [4], UROtsa cells (SV40-transformed human bladder epithelial line) [3], human lymphoblasts (M. Styblo, personal communication),

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“…233 This view is complemented by lack of consistent evidence for genotoxicity and carcinogenicity in nonmammalian systems, including the Ames test. [234][235][236][237][238] Antimony potassium tartrate is not mutagenic in the Ames bacterial reversion test and its carcinogenicity is unproven. 239 The limited studies in rodents suggesting a greater a female sensitivity to antimony-induced lung tumours are inadequate.…”

Section: Antimonymentioning

confidence: 99%

CHAPTER 17. Arsenic, Antimony and Bismuth

2013

Issues in Toxicology

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An assessment of the genetic toxicology of antimony trioxide

Cited by 29 publications

References 6 publications

Genotoxic risk and oxidative DNA damage in workers exposed to antimony trioxide

Genotoxic risk and oxidative DNA damage in workers exposed to antimony trioxide

Genetic Toxicology of Arsenic and Antimony

CHAPTER 17. Arsenic, Antimony and Bismuth

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