Genetic and environmental influences on baseline SCE

Abstract

Previous population-based studies have identified subject characteristics that, when combined, can account for approximately 20% of the observed interindividual variation in baseline SCE rates. In the present investigation, a classic twin study design was used to address the issue of the relevance of genetic factors to baseline SCE rates and to identify other demographic, hematologic, and exposure variables predictive of SCE rate. Questionnaire data and peripheral blood samples from 136 monozygotic and 88 dizygotic twins (age range: 25-81 years) were obtained. Among the large number of variables examined, univariate analyses (including ANOVA tests for the categorical variables and Pearson-product moment correlations for the quantitative variables) revealed smoking status, coffee drinking status, sex, white blood cell count, and absolute numbers of lymphocytes and neutrophils to have significant effects on SCE rates. A stepwise multiple regression analysis showed that together, smoking and coffee drinking status entered at the first step accounted for 21% of the observed variance in SCE, with a further 6% being contributed by the demographic and hematologic variables added in subsequent steps. Finally, the twin analyses showed that after adjustment of the data set for smoking and other significant predictors, genetic factors accounted for approximately 30% of the variation in SCE rates. Thus these data support the hypothesis of a significant genetic influence on baseline SCE.

XRCC1 , CYP2E1 and ALDH2 genetic polymorphisms and sister chromatid exchange frequency alterations amongst vinyl chloride monomer-exposed polyvinyl chloride workers

“…Age and smoking have been reported to account for about 30% of the variance in SCE frequency (Sarto et al 1985;Hirsch et al 1992). In this study, age and smoking accounted for about 10% of the variation, while VCM exposure contributed 20%.…”

“…Interestingly, genotypes explained about 10% of the variation in SCE. A previous study also showed that genetic factors accounted for about 30% of the variation in SCE frequency (Hirsch et al 1992). It will be intriguing to further investigate whether other genotypes contribute to the unexplained variation in SCE frequency.…”

Cytogenetic outcomes of adjuvant chemotherapy in non-target cells of breast cancer patients

“…Consequently, heritable differences in enzymes involved in oxidative metabolism and detoxifying systems can modify levels of induced DNA damage. 17 Individual cancer patients in our study showed different sensitivities and variations in clinical responses even to an identical scheme of chemotherapy, and we assume that it was strongly influenced by their personal genetic background and individual genome sensitivity. It was observed earlier that a small variation in the administered dose of anticancer drugs could lead to severe and life-threatening toxicity in some individuals and poor antitumor effects in others.…”

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

“…Drugi pak navode da HFC mogu biti subpopulacija dugoživućih limfocita u kojima se u uvjetima in vivo, tijekom G 0 -faze, nakuplja više oštećenja, pa prema tome imaju predispoziciju za veći broj SCE. Smatra se da visoke vrijednosti SCE utvrđene u ovim stanicama mogu odražavati kumulativno oštećenje genoma uzrokovano kroničnim izlaganjem mutagenima (125).…”

“…U nekim je istraživanjima dokazan porast učestalosti SCE s dobi (126,127). Žene općenito imaju nešto više vrijednosti SCE od muškaraca (125,127,128,129). Primijećeno je da učestalost SCE raste i tijekom trudnoće, što se pripisuje učinku hormona (130).…”