The Use of Biological Markers in Toxicology

Henderson, Rogene F.; Bechtold, William E.; Bond, James A.; Sun, James D.

doi:10.3109/10408448909017904

Cited by 134 publications

(51 citation statements)

References 67 publications

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“…enzyme induction). Biochemical events resulting from exposure to xenobiotics have been proposed as biomarkers, generally seen as 'changes in a biological system that can be related to an exposure to, or effect from, a specific xenobiotic or type of toxic material' (Henderson et aL, 1989).…”

Section: Introductionmentioning

confidence: 99%

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DNA adduct formation and 7-ethoxyresorufin O-deethylase induction in primary culture of rainbow trout hepatocytes exposed to benzo[a]pyrene

Masfaraud¹,

Devaux²,

Pfohl‐Leszkowicz³

et al. 1992

Toxicology in Vitro

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Abstract--The formation of DNA adducts, using the 32p-postlabeiling assay, and induction of 7-ethoxyresorufin O-deethylase (EROD) were investigated in a primary culture of rainbow trout hepatocytes exposed to benzo[a]pyrene (B[a]P). Concentrations of 0.1 and 1/zM-B[a]P were shown to induce EROD whereas 10 #M was an inhibitory concentration. DNA adducts were detected for 12 hr to 72 hr after exposure to 1 #M-B[a]P whereas EROD activity was increased 36 hr after treatment. The pattern of adducts was shown to be identical to that obtained after B[a]P treatment of rainbow trout in vivo, as demonstrated by co-chromatography of the adducts. Pre-exposure of hepatocytes for 48 hr to fl-naphthoflavone (~NF) and subsequent 24-hr exposure to 1 ~uM-B[a]P did not lead to increased DNA adduct formation although flNF treatment led to a 3.4-fold induction of EROD activity at the time of B[a]P addition. This study suggests that primary culture of rainbow trout hepatocytes provides a suitable method for studying DNA adduct formation and its modulating factors/n vitro.

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Section: Introductionmentioning

confidence: 99%

“…Xenobiotics may interact with DNA either directly or after transformation by metabolizing enzymes into reactive species that react with DNA forming DNA addition products (DNA adducts). Thus, DNA adducts were proposed as a biomarker of exposure to genotoxic compounds (Henderson et al, 1989;Perera, 1987).…”

Section: Introductionmentioning

confidence: 99%

DNA adduct formation and 7-ethoxyresorufin O-deethylase induction in primary culture of rainbow trout hepatocytes exposed to benzo[a]pyrene

Masfaraud¹,

Devaux²,

Pfohl‐Leszkowicz³

et al. 1992

Toxicology in Vitro

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show abstract

“…The actual target organ or cell is usually not available for measurements and biomarkers of exposure are thus often surrogate measures of doses or effects at the target. The ideal biomarker has been described as chemical-specific, detectable at low (trace) levels, available using non-invasive techniques, inexpensive to analyse and quantitatively related to prior exposures (Henderson et al, 1989). Thus, for biomonitoring purposes, biological materials should be easily accessible in sufficient amounts under routine conditions and without unacceptable discomfort and health risk for the individual.…”

Section: Discussionmentioning

confidence: 99%

CYP1A1 Gene Polymorphisms: Modulator of Genetic Damage in Coal-Tar Workers

Giri

Yadav²,

Kumar

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Aim: It is well known that polycyclic aromatic hydrocarbons (PAHs) such as benzo (a) pyrene have carcinogenic properties and may cause many types of cancers in human populations. Genetic susceptibility might be due to variation in genes encoding for carcinogen metabolizing enzymes, such as cytochrome P-450 (CYP450). Our study aimed to investigate the effect of genetic polymorphisms of CYP1A1 (m1 and m2) on genetic damage in 115 coaltar workers exposed to PAHs at their work place. Methods: Genetic polymorphisms of CYP1A1 were determined by the PCR-RFLP method. Comet and buccal micronucleus assays were used to evaluate genetic damage among 115 coal tar workers and 105 control subjects. Results: Both CYP1A1 m1 and CYP1A1 m2 heterozygous and homozygous (wt/mt+mt/mt) variants individually as well as synergistically showed significant association (P<0.05) with genetic damage as measured by tail moment (TM) and buccal micronuclei (BMN) frequencies in control and exposed subjects. Conclusion: In our study we found significant association of CYP1A1 m1 and m2 heterozygous (wt/mt)+homozygous (mt/mt) variants with genetic damage suggesting that these polymorphisms may modulate the effects of PAH exposure in occupational settings.

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“…The possible internal TDA exposures and effects when handling 2,4-TDA are detected from analysis of the substances in the urine, blood and plasma, and from the protein and DNA adducts (Bryant and Osterman-Golkar 1991;Henderson et al 1989). …”

Section: Selection Of Indicatorsmentioning

confidence: 99%

2,4‐Toluylene diamine [BAT Value Documentation, 2010]

Lewalter¹

2012

The MAK‐Collection for Occupational Health and Safety

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Published in the series BAT Value Documentations , Vol. 5 (2010) The article contains sections titled: Metabolism and Kinetics Critical Toxicity Exposure and Effect Selection of Indicators 2,4‐TDA in the urine 2,4‐TDA protein adducts DNA adducts Methods Background Exposure Evaluation of Biological Exposure Equivalents 2,4‐TDA in the urine 2,4‐TDA in protein adducts Evaluation of Biological Exposure Equivalents (EKA) Interpretation of Data

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The Use of Biological Markers in Toxicology

Cited by 134 publications

References 67 publications

DNA adduct formation and 7-ethoxyresorufin O-deethylase induction in primary culture of rainbow trout hepatocytes exposed to benzo[a]pyrene

DNA adduct formation and 7-ethoxyresorufin O-deethylase induction in primary culture of rainbow trout hepatocytes exposed to benzo[a]pyrene

CYP1A1 Gene Polymorphisms: Modulator of Genetic Damage in Coal-Tar Workers

2,4‐Toluylene diamine [BAT Value Documentation, 2010]

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