Comparison of ethylene, propylene and styrene 7,8-oxide in vitro adduct formation on N-terminal valine in human haemoglobin and on N-7-guanine in human DNA

Pauwels, W; Veulemans, Hendrik

doi:10.1016/s1383-5718(98)00106-5

Cited by 37 publications

(19 citation statements)

References 31 publications

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“…In mammals, EO can also be metabolically produced from ethylene. Both oxidation processes are mediated by the cytochrome P450 monooxygenase system (IARC, 2002;Pauwels and Veulemans, 1998;Sumner and Fennell, 1994;Filser and Bolt, 1983). DNA damage induced by SO and EO is considered to be caused by alkylation of DNA bases, while G causes DNA breaks directly via one-electron oxidation or indirectly through the OH-radical (IARC, 1994(IARC, , 2002.…”

Section: Gstt1mentioning

confidence: 99%

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

et al. 2006

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Section: Gstt1mentioning

confidence: 99%

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

et al. 2006

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“…The fate of styrene in humans with respect to uptake and disposition is well understood [IARC, 2002;Pauwels and Veulemans, 1998;Sumner and Fennell, 1994]. The first step in the metabolic pathway is the formation of SO mediated by the cytochrome P450 (CYP)-mediated monooxygenase system.…”

Section: Introductionmentioning

confidence: 99%

Influence of genetic polymorphisms on biomarkers of exposure and genotoxic effects in styrene‐exposed workers

Godderis

Boeck

Haufroid

et al. 2004

Environ and Mol Mutagen

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A study on 44 workers exposed to styrene and 44 matched referents was performed in order to examine the influence of genetic polymorphisms in biotransformation and DNA repair enzymes on the levels of N-terminal hemoglobin adducts and genotoxicity biomarkers. Urinary mandelic acid concentration averaged 201.57 mg/g creatinine +/-148.32 in exposed workers, corresponding to a calculated average airborne styrene exposure of 9.5 ppm +/-9.6. Individuals with a high level of N-terminal valine adducts had higher levels of DNA damage, as evaluated by the Comet assay (r = 0.29, P = 0.008). Frequencies of micronucleated mononucleated lymphocytes (MNMC) (0.71 +/- 0.88 vs 0.11 +/- 0.20, P<0.0001), micronucleated binucleated lymphocytes (MNBC) (3.93 +/- 2.75 vs 2.65 +/- 1.94, p = 0.02) and micronucleated nasal epithelial cells (0.52 +/- 0.49 vs 0.23 +/- 0.31, p = 0.04) differed significantly between the exposed and referent groups. In the whole group of 88 individuals, higher frequencies of MNMC were found in individuals possessing the XRCC3 Met(241) allele and those individuals with the XRCC1 Gln( (399) ) allele showed higher frequencies of MNMC and MNCB. In vitro DNA repair capacity, as measured by residual DNA strand breaks in peripheral blood leukocytes after a styrene oxide challenge, was also influenced by styrene exposure, with an apparent induction of early repair mechanisms associated with the intensity of recent exposure and a reduction of late (24 h) repair capacity that was associated with the duration of employment. After 1 h of repair, lower levels of residual DNA damage were found in individuals possessing GSTT1 (P = 0.043). After 24 h of repair, lower residual DNA damage was found in individuals homozygous for XRCC1 Arg(194) (P = 0.013). Multivariate regression analysis indicated that the duration of exposure, smoking habits and polymorphisms of XRCC1 at codon 399 were important variables affecting the genotoxic responses. Our data suggest that DNA damage is formed in workers exposed to low concentrations of styrene, and that genotypes of metabolising and DNA-repair genes are important for the assessment of individual genotoxic risk to styrene. The in vitro DNA repair phenotype assay might be a valuable method to estimate the susceptibility of workers.

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“…The efficiency of alkylation in mice is only half of that found in rats and dogs (IARC 1994). The chemical reactivity of 1,2-epoxypropane is four times lower than that of ethylene oxide (Pauwels and Veulemans 1998). There is evidence of the enantioselective reactivity of the two optical isomers (Peter et al 1991); all studies were, however, carried out with the racemate of 1,2-epoxypropane.…”

Section: Repeated Exposurementioning

confidence: 99%

1,2‐Epoxypropane [MAK Value Documentation, 2013]

2015

The MAK‐Collection for Occupational Health and Safety

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The article contains sections titled: Toxic Effects and Mode of Action Mechanism of Action Toxicokinetics and Metabolism Absorption, distribution, elimination Metabolism Effects in Humans Single exposures Repeated exposure Local effects on skin and mucous membranes Allergenic effects Reproductive and developmental toxicity Genotoxicity Carcinogenicity Animal experiments and in vitro studies Acute toxicity Subacute, subchronic and chronic toxicity Local effects on skin and mucous membranes Allergenic effects Reproductive and developmental toxicity Genotoxicity Carcinogenicity Manifesto (MAK value/classification)

show abstract

Comparison of ethylene, propylene and styrene 7,8-oxide in vitro adduct formation on N-terminal valine in human haemoglobin and on N-7-guanine in human DNA

Cited by 37 publications

References 31 publications

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

Influence of genetic polymorphisms on biomarkers of exposure and genotoxic effects in styrene‐exposed workers

1,2‐Epoxypropane [MAK Value Documentation, 2013]

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