Sister-chromatid exchanges in cigarette-smoking human females and their newborns

Ardito, G.; Lamberti, Laura; Ansaldi, E; Ponzetto, Paola

doi:10.1016/0165-1218(80)90100-7

Cited by 86 publications

(26 citation statements)

References 11 publications

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“…Recent studies of SCE rates in peripheral lymphocytes in cigarette smokers have demonstrated normal SCE rates (HOLLANDER et al 1978; MERETOJA et al 1978; ARDITO et al 1980;CROSSEN and MORGAN 1980) or increased SCE rates (LAM- BERT et al 1978;VALADAUD-BARRIEU and IZARD 1979; HOPKIN and EVANS 1980;HUSGAFVEL-PURSIAI-NEN et al 1980). In all of these studies except the study by CROSSEN and MORGAN (1980) the number of healthy individuals examined was considerably lower than in the present study.…”

Section: Methodsmentioning

confidence: 99%

“…Since lung cancer is known to be strongly associated with cigarette smoking, the question of a possible association between SCE and cigarette smoking is of interest. However, both normal SCE rates (HOLLANDER et al 1978;MERETOJA et al 1978;ARDITO et al 1980;CROSSEN and MORGAN 1980) and increased SCE rates (LAMBERT et al 1978;VALADAUD-BARIEU and IZARD 1979;HOPKIN and EVANS 1980;HUSGAFVEL-PURSIAINEN et a]. 1980) have been reported in cigarette smokers.…”

Section: Bent Husum Department Of Anesthesia Gentofte Hospital Dk-mentioning

confidence: 99%

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Increased sister chromatid exchange frequency in lymphocytes in healthy cigarette smokers

Husum

Wulf²,

Niebuhr³

2008

Hereditas

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SCE rates in peripheral lymphocytes may be useful for evaluation of environmental mutagens. Since lung cancer is strongly associated with cigarette smoking, an association of SCE with cigarette smoking might be of interest. Controversy about this question prompted the present study of SCE in peripheral lymphocytes in 149 healthy, unmedicated persons. 60 non‐smokers had 8.25 ± 0.13 SCE/cell (mean value ± standard error of the mean), and 89 cigarette smokers had 9.23 ± 0.14 SCE/cell. The sum of SCE in 30 metaphases in each person was transformed to a normally distributed metameter, y= (SCE)½+ (SCE+1)½, which was found to be significantly increased with increasing cigarette consumption. The linear regression calculated for y= (SCE)½+(SCE+1)½ and x=number of cigarettes smoked per day was y=31.43+0.094 x. It was concluded that cigarette smokers have increased SCE in peripheral lymphocytes. The significance of this in respect to risk of development of cancer in the lung is unknown. The influence of cigarette smoking should be considered when using the SCE test principle to evaluate in vivo exposure to potential mutagens.

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Section: Methodsmentioning

confidence: 99%

Section: Bent Husum Department Of Anesthesia Gentofte Hospital Dk-mentioning

confidence: 99%

Increased sister chromatid exchange frequency in lymphocytes in healthy cigarette smokers

Husum

Wulf²,

Niebuhr³

2008

Hereditas

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“…On the other hand, no correlation between smoking and SCE incidence has been revealed in a number of studies (2,7,13,17,29,30).…”

Section: Sister Chromatid Exchange and Smokingmentioning

confidence: 99%

Chromosome changes in workers (smokers and nonsmokers) exposed to automobile fuels and exhaust gases.

Fredga¹,

Davring²,

Sunner³

et al. 1982

Scand J Work Environ Health

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“…Unlike chromosomal aber- (A) Three studies using low levels of 5-bromo-2-deoxyuridine (BUdR) in the culture media. Data are from (31)(32)(33). Frequencies of sister chromatid exchanges were consistently higher in maternal than in fetal cells.…”

Section: Chromosomalmentioning

confidence: 99%

“…Data from four studies (31)(32)(33)(34) evaluating the frequencies of sister chromatid exchanges among women who smoked during pregnancy and cord blood specimens from their offspring are presented in Figure 1. Each of these studies found appreciably lower rates of sister chromatid exchanges in cord blood lymphocytes than in maternal blood lymphocytes.…”

Section: Chromosomalmentioning

confidence: 99%

A review of approaches to the detection of genetic damage in the human fetus.

Everson

1987

Environ Health Perspect

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Studies in experimental animals suggest links between genetic damage to the fetus and the etiology of several disorders, including fetal loss, teratogenesis, and cancer. Methods for measuring genetic damage directly in the human fetus could provide epidemiologists and clinical researchers with powerful tools for investigating similar associations in humans. Current methods potentially available for such studies include assays for mutagenic substances in human body fluids and for measuring modifications to genetic material at the three levels of organization of genetic material: the chromosome, the gene or specific locus, and chemical DNA. Results of studies using fetal tissues to investigate each of these end points are reviewed, emphasizing studies of chemical modifications to DNA nucleotides detected in the human placenta.

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Sister-chromatid exchanges in cigarette-smoking human females and their newborns

Cited by 86 publications

References 11 publications

Increased sister chromatid exchange frequency in lymphocytes in healthy cigarette smokers

Increased sister chromatid exchange frequency in lymphocytes in healthy cigarette smokers

Chromosome changes in workers (smokers and nonsmokers) exposed to automobile fuels and exhaust gases.

A review of approaches to the detection of genetic damage in the human fetus.

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