Urinary cyclophosphamide excretion and micronuclei frequencies in peripheral lymphocytes and in exfoliated buccal epithelial cells of nurses handling antineoplastics

Burgaz, Sema; Karahalıl, Bensu; Bayrak, Pinar; Taşkın, Lale; Yavuzaslan, Fadime; Bökesoy, Işık; Anzion, Rob; Bos, R.P.; Platin, Nurgün

doi:10.1016/s1383-5718(98)00180-6

Cited by 111 publications

(67 citation statements)

References 35 publications

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“…Some biomonitoring studies found positive association of age (Ozkul et al,1997;Moretti et al, 2000), sex (Betti et al, 1994;Bajpayee et al, 2002;Fenech et al, 2003), smoking (Burgaz et al, 1999;Hoffmann et al, 2005), alcohol intake (Ramirez et al, 2002) and tobacco chewing (Nair et al, 1991;Trivedi et al, 1993) while some studies observed no association of age (Zhu et al, 1999;Konapaka et al, 2003), sex (Anderson et al, 1993;Zhu et al, 1999;Konapaka et al, 2003), smoking (Moller et al, 2006), alcohol intake (Celik et al, 2007;Martinez-Valenzuela et al, 2009) with genetic damage. In our study, we did not observe any significant association of age, sex and consumption habits (smoking and alcohol use) with genetic damage.…”

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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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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“…MN were determined in 16 studies. Effects of exposure were observed with PAHs (18,19), benzene (28), epichlorohydrin (40), pesticides (44), fluorides (47), cytostatics (50), and cosmic radiation (54). No effects were induced by VOCs (23,24), benzene (26,33), styrene (36), BD (37), malathion (46), or cosmic radiation (55).…”

Section: Discussionmentioning

confidence: 99%

“…Rubes et al (49), using FISH with painting probes specific for chromosomes 1 and 4, found significant differences in the number of translocations (p < 0.01), as well as in CAs determined by conventional methods, between an exposed group and controls (p < 0.05). Burgaz et al (50) observed in a group of nurses an increase of MN frequencies in peripheral lymphocytes and in buccal epithelial cells. Using the Comet assay, Undeger et al (51) found that DNA damage was greater in nurses than in controls and that this effect was smaller in nurses using individual safety protection during their work.…”

mentioning

confidence: 95%

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

Srám¹,

Binková²

2000

Environmental Health Perspectives

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Molecular epidemiology is a new and evolving area of research, combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and influence of individual susceptibility with epidemiologic methodologies. Biomarkers evaluated were selected according to basic scheme: biomarkers of exposure-metabolites in urine, DNA adducts, protein adducts, and Comet assay parameters; biomarkers of effect-chromosomal aberrations, sister chromatid exchanges, micronuclei, mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, and the activation of oncogenes coding for p53 or p21 proteins as measured on protein levels; biomarkers of susceptibility-genetic polymorphisms of genes CYP1A1, GSTM1, GSTT1, NAT2. DNA adducts measured by 32P-postlabeling are the biomarker of choice for the evaluation of exposure to polycyclic aromatic hydrocarbons. Protein adducts are useful as a biomarker for exposure to tobacco smoke (4-aminobiphenyl) or to smaller molecules such as acrylonitrile or 1,3-butadiene. Of the biomarkers of effect, the most common are cytogenetic end points. Epidemiologic studies support the use of chromosomal breakage as a relevant biomarker of cancer risk. The use of the Comet assay and methods analyzing oxidative DNA damage needs reliable validation for human biomonitoring. Until now there have not been sufficient data to interpret the relationship between genotypes, biomarkers of exposure, and biomarkers of effect for assessing the risk of human exposure to mutagens and carcinogens. Key words: air pollution, benzene, biomarkers, coke oven, genotypes, occupational exposure, PAHs, pesticides, tobacco smoke. -Envwron Health Perspect 1 08(suppl 1):57-70 (2000). http.//ehpnetl. niehs. nih.gov/docs/2000/suppl-1/57-70sram/abstract. html A new and evolving area of research termed molecular epidemiology attempts to merge sophisticated and highly sensitive laboratory methods (many of them developed during the recent revolution in molecular biology) with analytical epidemiologic methods. Molecular epidemiology bridges basic research in molecular biology and studies of human cancer causation by combining laboratory measurement of internal dose, biologically effective dose, biologic effects, and the influence of individual susceptibility with epidemiologic methodologies (1). The most common view is that the approach represents a natural convergence of molecular biology and epidemiology (2).The number of biomarkers available for evaluating genetic and cancer risk in humans is quite large. Their utility-for human biomonitoring is suggested by the well-known paradigm of environmentally induced cancer, which represents end points for assessing the entire spectrum of human-genotoxicant interactions (3). These biomarkers begin with exposure and include absorption, metabolism, distribution, critical target interaction (i.e., DNA damage and repair), genetic changes, and finally, disease, which is the province of traditional epidemiology. The development of biomarkers has given rise to the field of ...

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“…Rezultati istraživanja provedenih u različitim državama, uključujući i Hrvatsku (69,72,79,98), prikazani su na tablici 3. U većini istraživanja primijenjen je MN-test na limfocitima periferne krvi, a u njih šest na epitelnim stanicama bukalne sluznice (92,93,97,99,106,107). Iz odnosa broja istraživanja koja su primjenom MN-testa dobila pozitivne i/ili negativne rezultate (slika 6) vidljiv je bolji omjer nego u ostalih citogenetičkih metoda, koji upućuje na osjetljivost tehnike i njezinu dobru primjenjivost u nadzoru nad osobljem koje rukuje antineoplastičnim lijekovima.…”

Section: Mn-testunclassified

Antineoplastic Drugs as a Potential Risk Factor in Occupational Settings: Mechanisms of Action at the Cell Level, Genotoxic Effects, and Their Detection Using Different Biomarkers

Kopjar

Želježić

Kašuba

et al. 2010

Archives of Industrial Hygiene and Toxicology

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Nevenka KOPJAR, Davor ŽELJEŽIĆ, Vilena KAŠUBA i Ružica ROZGAJ Institut za medicinska istraživanja i medicinu rada, Zagreb, HrvatskaPrimljeno u siječnju 2010. Prihvaćeno u veljači 2010.U članku je prikazana osnovna podjela antineoplastičnih lijekova prema mehanizmima djelovanja na razini stanice. Objašnjeni su mehanizmi genotoksičnosti najvažnijih vrsta lijekova koji se primjenjuju u okviru uobičajenih protokola za liječenje zloćudnih novotvorina. Navedena je važeća klasifi kacija antineoplastika prema kancerogenom potencijalu, podaci o mutagenom potencijalu te je prikazana njihova podjela u skladu s anatomsko-terapijsko-kemijskim sustavom klasifi kacije. Sustavno su prikazani najvažniji rezultati svjetskih i hrvatskih istraživanja na populacijama radnika izloženih antineoplasticima, provedenih u razdoblju 1980.-2009. s pomoću četiri najčešće primjenjivane metode: analize izmjena sestrinskih kromatida, analize kromosomskih aberacija, mikronukleus-testa i komet-testa. Objašnjena su osnovna načela navedenih metoda te raspravljene njihove prednosti i nedostaci. Biološki pokazatelji daju važne podatke o individualnoj osjetljivosti profesionalno izloženih ispitanika koji mogu poslužiti unaprjeđenju postojećih uvjeta rada i upravljanju rizicima pri izloženosti genotoksičnim agensima. Na osnovi prednosti i nedostataka citogenetičkih metoda zaključeno je da je mikronukleus-test, koji podjednako uspješno dokazuje klastogene i aneugene učinke, jedna od najboljih metoda dostupnih za otkrivanje štetnih djelovanja antineoplastičnih lijekova koji su u aktivnoj primjeni.

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Urinary cyclophosphamide excretion and micronuclei frequencies in peripheral lymphocytes and in exfoliated buccal epithelial cells of nurses handling antineoplastics

Cited by 111 publications

References 35 publications

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

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

Molecular Epidemiology Studies on Occupational and Environmental Exposure to Mutagens and Carcinogens, 1997-1999

Antineoplastic Drugs as a Potential Risk Factor in Occupational Settings: Mechanisms of Action at the Cell Level, Genotoxic Effects, and Their Detection Using Different Biomarkers

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