Analysis of chromosomes of workers exposed to acrylonitrile

Thíess, A. M.; Fleig, I

doi:10.1007/bf00302526

Cited by 33 publications

(10 citation statements)

References 4 publications

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“…The disagreement between the significance of the sister chromatid exchange frequency observed in this study and the lack of chromosome aberrations in lymphocytes of acrylonitrile-exposed workers (14) is probably due to differences in experimental conditions and acrylonitrile doses « 20 ppm for the exposed workers).…”

Section: Referencescontrasting

confidence: 77%

“…This monomer is widely used as an intermediate in the manufacture of synthetic fibers, plastics, and rubbers and as a grain fumigant, and it has been shown to have mutagenic power in assay systems utiliz-0355-3140/82/040290-04USD2.00 ing bacterial cells (7,17) and carcinogenic activity in animals (6,15,16). Furthermore, acrylonitrile is toxic and a suspected carcinogen to man (4), even if negative results have been obtained concerning its genotoxic action in cytogenetic studies on mice and rats (11) and in epidemiologic investigations carried out with exposed workers (14).…”

mentioning

confidence: 99%

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Increase of sister chromatid exchange and unscheduled synthesis of deoxyribonucleic acid by acrylonitrile in human lymphocytes in vitro.

Perocco¹,

Pane²,

Zannotti³

1982

Scand J Work Environ Health

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, MS2PEROCCO P, PANE G, BOLOGNESI S, ZANNOTTI M. Increase of sister chromatid exchange and unscheduled synthesis of deoxyribonucleic acid by acrylonitrile in human. lymphocytes in vitro. Scand j work environ health 8 (1982) 290-293. The investigation. has been carried out on cultures grown in the presence of 5 x 10-1 -5 X 10-5 M acrylonitrile with or without a rat liver metaboli2ing system (S-9 mix). The results obtained showed that acrylonitrile was toxic starting from the 5 x 10-3 M concentration, caused a significant increase in the sister chromatid exchange (SCE) frequency in comparison with the controls (p ::; 0.00l) when the concentration was 5 x 10-4 M, and elicited reparative deoxyribonucleic acid (DNA) synthesis, determined by tritiated thymidine uptake, particularly when the concentration was 5 x 10-1 M. These effects were observed in lymphocytes of different donors and after drug activation by the S-9 mix metaboli2ing system.

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Section: Referencescontrasting

confidence: 77%

mentioning

confidence: 99%

Increase of sister chromatid exchange and unscheduled synthesis of deoxyribonucleic acid by acrylonitrile in human lymphocytes in vitro.

Perocco¹,

Pane²,

Zannotti³

1982

Scand J Work Environ Health

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“…Early epidemiological studies have suggested that AN may increase the incidence of lung, colon, and stomach cancers among exposed workers (Thiess and Fleig, 1978;Blair et al, 1998). However, recent studies suggested that there is no significant association between human exposure to AN and carcinogenicity (Benn and Osborne 1998;Swaen et al, 1998;Wood et al, 1998;IARC, 1999;Marsh et al, 2001;Schulz et al, 2001).…”

Section: Acrylonitrile (Anmentioning

confidence: 99%

Cytochrome P450 2E1 (CYP2E1) is Essential for Acrylonitrile Metabolism to Cyanide: Comparative Studies Using CYP2E1-Null and Wild-Type Mice

Wang

Chanas²,

Ghanayem³

2002

Drug Metab Dispos

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ABSTRACT:Acrylonitrile (AN) is a rodent carcinogen and suspected human carcinogen. Metabolism of AN proceeds via conjugation with glutathione or epoxidation via cytochrome P4502E1 (CYP2E1) to cyanoethylene oxide (CEO). It was hypothesized that CEO metabolism via epoxide hydrolase (EH) is the primary pathway for cyanide formation. The objective of this work is to assess the enzymatic basis of metabolism to cyanide. Male wild-type and CYP2E1-null mice received 0, 2.5, 10, 20, or 40 mg of AN/kg by gavage, and cyanide was measured in blood and tissues. CYP2E1 and EH expression were assessed using Western blot analyses. Present results demonstrated that cyanide concentrations in blood and tissues of AN-treated wild-type mice were higher at 1 versus 3 h, increased in a dose-dependent manner, and were significantly higher in AN-treated versus vehicle-treated mice. In contrast, cyanide concentrations in the blood and tissues of AN-treated CYP2E1-null mice were not statistically different from those of vehicle-treated mice. Furthermore, this work showed that EH is expressed in CYP2E1-null and wild-type mice. In conclusion, under the current experimental conditions using CYP2E1-null mice, current work demonstrated for the first time that CYP2E1-mediated oxidation is a prerequisite for AN metabolism to cyanide. Since earlier studies showed that CYP2E1 is the only enzyme responsible for AN epoxidation, it is concluded that AN metabolism to CEO is a prerequisite for cyanide formation, and this pathway is exclusively catalyzed by CYP2E1. Finally, this work confirmed that cyanide plays an essential role in the causation of the acute toxicity/mortality of AN.

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“…However, there are no reliable in vivo data supporting positive mutagenicity of AN to humans and mammals. Thiess and Fleig (1978) 66) studied whether of not chromosomal aberrations of peripheral lymphocytes would increase in workers exposed to 1.5-5 ppm (estimated levels) of AN for an average of 10-15 years, and found no changes in the incidence of chromosomal aberrations. Rabello-Gay and Ahmed (1980) 67) showed that treatment of mice orally with 7-21 mg/kg/day of AN for 4-30 days did not result in increased chromosomal aberrations of bone marrow cells.…”

Section: Mutagenicitymentioning

confidence: 99%

Carcinogenicity and Other Health Effects of Acrylonitrile with Reference to Occupational Exposure Limit.

SAKURAI

2000

INDUSTRIAL HEALTH

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The occupational exposure limit for acrylonitrile (AN) has been set by many organizations on the basis of its carcinogenicity. However, recent epidemiological studies do not afford evidence supporting the hypothesis that AN is carcinogenic to humans. Review of the 18 published cohort studies revealed that, although there is not adequate evidence in humans for carcinogenicity of AN, the possibility of a causal association between high exposure to AN and lung cancer in humans cannot be excluded. It was pointed out that carcinogenic potential of AN may be weak, if any, to humans, and the current occupational exposure limit (OEL) for AN of 2 ppm was evaluated as appropriate in view of AN exposure levels reported by epidemiological studies. Based also on review of the literature on health effects other than carcinogenicity, it was concluded that the current OEL for AN is a reasonable value and there is no need for a revision at present.

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Analysis of chromosomes of workers exposed to acrylonitrile

Abstract: Examination of 18 workers who had been exposed to acrylonitrile for 15.3 years on average and 18 workers who had not been exposed to acrylonitrile showed no difference in the incidence of chromosome aberrations; for each person concerned 100 metaphases were evaluated.

Cited by 33 publications

References 4 publications

Increase of sister chromatid exchange and unscheduled synthesis of deoxyribonucleic acid by acrylonitrile in human lymphocytes in vitro.

Increase of sister chromatid exchange and unscheduled synthesis of deoxyribonucleic acid by acrylonitrile in human lymphocytes in vitro.

Cytochrome P450 2E1 (CYP2E1) is Essential for Acrylonitrile Metabolism to Cyanide: Comparative Studies Using CYP2E1-Null and Wild-Type Mice

Carcinogenicity and Other Health Effects of Acrylonitrile with Reference to Occupational Exposure Limit.

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