Variation in sister-chromatid exchange among 106 members of the general U.K. population

Dewdney, R.S.; Lovell, D.; Jenkinson, P.C.; Anderson, Diana

doi:10.1016/0165-1218(86)90007-8

Cited by 52 publications

(7 citation statements)

References 28 publications

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“…Several large sample studies (each including more than 100 subjects) have explored the relationships between background variables and baseline SCE rates [Bender et al, 1988[Bender et al, , 1989Dewdney et al, 1986;Husum et al, 1986;Soper et al, 19841. Three variables examined in all of these investigations were: ( 1) cigarette smoking status, which consistently emerged as the subject characteristic having the 0 1992 Wiley-Liss, Inc. largest independent effect on baseline SCE rates, (2) sex, with females showing moderately higher mean SCE rates than males, and (3) age, which appeared to have a small effect independent of smoking status and sex in two of the four investigations [Husum et al, 1986;Soper et al, 19841. The only additional factor documented to correlate with SCE rates was white blood cell count in the Brookhaven-Oak Ridge laboratories collaborative study [Bender et al, 1988, 19891.…”

Section: Introductionmentioning

confidence: 99%

Genetic and environmental influences on baseline SCE

Hirsch

Sentz²

1992

Environ and Mol Mutagen

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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.

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Section: Introductionmentioning

confidence: 99%

Genetic and environmental influences on baseline SCE

Hirsch

Sentz²

1992

Environ and Mol Mutagen

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“…neous and chemically-induced genetic damage, as measured The existence of substantial interindividual variation in the frequencies of both spontaneous and chemicallyinduced chroniosome breakage (CB) and sister chromatid exchange (SCE) has; been well documented [Morgan and Crossen, 1977;Pero et al, 1978;Galloway and Wolff, 1979;Hedner et al, 1982;Dai et al, 1986;Dewdney et al, 1986;Bender et al, 19881. Although the effects of chemical clastogens have been noted for both of these parameters [Pero et al, 1978;Natarjan et al, 19821, there has been little progress in analyzing if and how spontaneous and chemically-induced SCE and CB frequencies are related, and ultimately, controlled.…”

Section: Introductionmentioning

confidence: 99%

Factors underlying variation in spontaneous and clastogen‐induced sister chromatid exchanges and chromosome breakage frequencies

Wasserman

Cohen

Schwartz

et al. 1990

Environ and Mol Mutagen

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The latent "factors" influencing spontaneous and clastogen-induced genetic damage, measured by rates of sister chromatid exchange (SCE) and chromosome breakage (CB), were investigated in a small sample of 20 unrelated, healthy individuals. The covariation of spontaneous and clastogen-induced (bleomycin [BLM], streptonigrin [SN], mitomycin-C [MMC], 4-nitroquinoline-1-oxide [4NQO]) SCEs and CBs was analyzed by maximum-likelihood factor analysis. A single-factor model resulted in large standardized regression coefficients of measured variables on the factor for spontaneous and BLM- and SN-induced SCE frequencies, and a modest regression coefficient for MMC-induced SCEs. A two-factor model, after varimax rotation, yielded one factor strongly associated with spontaneous and BLM- and SN-induced SCE frequencies, and a second factor associated with spontaneous and BLM- and SN-induced CBs. A bootstrap analysis of this data set indicated the statistical significance of one regression coefficient (i.e., P less than or equal to 0.05) and borderline significance (0.07 less than or equal to P less than or equal to 0.11) of three other regression coefficients on the first factor, to be interpreted as an effector of SCE frequencies. However, for the second factor, none of the bootstrapped regression coefficients was significant (P greater than 0.22). Due to the modest sample utilized in this study, the validity of this model should be further explored using additional, larger data sets.

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“…There was a significant difference between Comet responses between males and females from The Gambia, but only when male individual B13 was excluded from analysis, and not taking into account other sources of variability. Gender differences have been shown on previous occasions for other endpoints in other human monitoring studies measuring chromosome damage, SCE, proliferative rate index, mitogen-induced blastogenesis, vitamin C levels, and antioxidant capacity [22][23][24][25].…”

Section: Discussionmentioning

confidence: 76%

Aflatoxin exposure and DNA Damage in the comet assay in individuals from The Gambia, West Africa

Anderson

et al. 1999

Teratog. Carcinog. Mutagen.

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The single cell gel electrophoresis assay (Comet assay) was used to measure DNA damage in peripheral lymphocytes from a group of individuals from The Gambia in order to determine whether such damage could be associated with increased exposure to aflatoxin in this population. Responses obtained were correlated to responses previously obtained [1] in a cross‐sectional study in the same individuals of various cytogenetic alterations [chromosomal aberrations, micronuclei (crest positive and negative staining), and sister chromatid exchanges], and aflatoxin‐albumin adducts. Analysis of variance methods were used to assess the effects of smoking, GSTM1 genotype, sex, age, and smoking status. A comparison was also made between The Gambian individuals and a group of healthy, non‐smoking volunteers in the United Kingdom where aflatoxin exposure would be expected to be low. From the earlier study [1], it was determined that the levels of the sister chromatid exchanges and micronuclei were higher in The Gambian group than in a European group where aflatoxin exposure was lower, but that there were no correlations between the adduct levels and the cytogenetic abnormalities at the individual level. In the present study, DNA damage as measured in the Comet assay was not significantly higher than in the healthy United Kingdom volunteers. In addition, there were no associations between cytogenetic damage, GSTM1 genotype, age, sex, lifestyle factors (smoking and aflatoxin exposure), and Comet response at the individual level. Comet response was higher in females than males in The Gambia if one outlier was excluded from analysis and not taking into account other sources of variability. It would appear that DNA damage as measured in the Comet assay in peripheral blood lymphocytes is not a sensitive genotoxic marker of aflatoxin exposure in this population. Teratogenesis Carcinog. Mutagen. 19:147–155, 1999. © 1999 Wiley‐Liss, Inc.

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Variation in sister-chromatid exchange among 106 members of the general U.K. population

Cited by 52 publications

References 28 publications

Genetic and environmental influences on baseline SCE

Genetic and environmental influences on baseline SCE

Factors underlying variation in spontaneous and clastogen‐induced sister chromatid exchanges and chromosome breakage frequencies

Aflatoxin exposure and DNA Damage in the comet assay in individuals from The Gambia, West Africa

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