Chromosome Aberrations Induced in Cultured Human Cells by Caffeine

Lee, Sung

doi:10.1266/jjg.46.337

Cited by 28 publications

(5 citation statements)

References 16 publications

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“…Dicentric chromosomes, which given rise to sister-cell fusion, result from the rejoining of broken chromosomes, and caffeine induces extensive breakage (Kihlman, 1977). However, these breaks do not readily rejoin, so that the incidence of exchange aberrations is low; most of the aberrations detected are breaks, gaps, and acentric fragments (Ostertag et al, 1965;Lee, 1971;Kihlman et al, 1971), at least at concentrations below 25 mM. Furthermore, it is by no means established that the lethal effects we have described here derive from such chromosomal damage: although the incidence of fusion becomes very high with the higher concentrations of caffeine, most of the cells die before they hse, so that few are at risk.…”

Section: Discussionmentioning

confidence: 99%

Growth and death of hela cells in the presence of caffeine

Beetham

Tolmach

1982

Journal Cellular Physiology

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Proliferation and death were measured in synchronously growing cultures of HeLa S3 cells during treatment with up to 30 mM caffeine. Changes in the number of colony-forming cells were determined by single-cell plating, while changes in the total number of cells were measured both by electronic counting and by monitoring cell division and physiological death cinemicrographically. At concentrations between 2 and 5 mM, cell killing occurs over several days during which the cells traverse the generation cycle once or a few times before losing colony-forming ability, with consequent proliferation of non-colony-forming cells. This indicates that lethal damage is accumulated with time. Death occurs more rapidly at higher concentrations, without proliferation, the kinetics of inactivation being strongly dependent on the phase of the cycle (cell age) at which treatment is initiated. G1 cells are killed more slowly in 10 mM caffeine than are S cells, but G1 cells respond rapidly to 20 mM caffeine, suggesting the inception of an additional mode of killing. The incidence of sister-cell fusion increases with increasing caffeine concentration above 1 mM. On addition of 10 mM caffeine to a culture prepared from collected mitotic cells, the cells undergo a transient rounding and then respread after several hours; with 20 mM, they never respread. The generation cycle is prolonged in a concentration-dependent fashion, as is the duration of G1; the generation time is doubled in 5-6 mM caffeine. G2 and M are also prolonged at concentrations above 3 mM, but S is not prolonged even by 10 mM caffeine.

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Section: Discussionmentioning

confidence: 99%

Growth and death of hela cells in the presence of caffeine

Beetham

Tolmach

1982

Journal Cellular Physiology

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“…More recently, a high frequency of chromatid aberrations, predominantly of the unstable type, has been induced with caffeine in human leucocytes and human embryonic cells in culture (Lee, 1971). Studies on the fate of radiationinduced chromosome aberrations (Buckton, Jacobs, Court Brown & Doll, 1962;Norman, Sasaki, Ottoman & Fingerhut, 1966;Sasaki & Norman, 1967;Leonard, 1970) have shown that such unstable aberrations do not survive cell divisions due to the genetic imbalance caused by the abnormal distribution of genetic material to the daughter cells.…”

Section: Discussionmentioning

confidence: 99%

Effect on the Offspring of Repeated Caffeine Administration to Pregnant Rats

Gilbert¹,

Pistey²

1973

Reproduction

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Repeated intraperitoneal injections of caffeine given to rats in dosages ranging from 4 to 16 mg daily throughout pregnancy resulted in significant resorptions and decrease in the birth weight ofthe offspring. These effects were dose-related. Developmental malformations, however, were not observed in the offspring at these dosage levels. These results indicate that caffeine, even in low doses which at the lower levels of the experiment may approximate to the daily human intake of a heavy coffee consumer, suppresses growth of embryonic and fetal tissues.

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“…Chronic exposure to caffeine also induced a significant increase in the frequency of SCEs. The lowest effective concentration of caffeine used, 0.25 mM, was approximately one-tenth of that needed to cause a significant increase in the frequency of chromosomal aberrations in similar experiments [Lee, 1971;Weinstein et al, 1972, 19751. No increase in SCEs was observed when caffeine (3.1-5.1 mM) was administered acutely immediately after the addition of PHA.…”

Section: Discussionmentioning

confidence: 76%

“…Caffeine has been extensively examined for possible genetic effects in a variety of eukaryotic systems (see [Kihlman, 1977; Legator and Zimmering, 1979; Thayer and Palm, 1975; Timson, 1977; Ostertag et al, 19651 for reviews). Caffeine's ability to induce chromosomal aberrations in vitro is well documented [Kihlman, 1977; Legator and Zimmering, 1979; Thayer and Palm, 1975; Timson, 1977; Ostertaget al, 1965; Kuhlmann et al, 1968; Lee, 1971; Weinstein et al, 1972; Timson, 19701, whereas its ability to induce SCE is equivocal. In an experiment designed to examine caffeine's ability to inhibit the induction of SCEs by ultraviolet light in Chinese hamster ovary cells, caffeine alone had no effect on SCE levels [Kato, 19731. Since that initial report, several investigators have examined the effect of caffeine treatment on potentiating or suppressing SCE induction by a variety of DNA-damaging agents.…”

Section: Introductionmentioning

confidence: 99%

Induction of sister chromatid exchanges and inhibition of cellular proliferation in vitro. I. caffeine

1982

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Cytogenetic assay systems based on the detection of sister chromatid exchanges (SCE) are widely advocated as a sensitive screening method for assessing genotoxic potential. While many agents have been examined for their ability to induce SCE's, complete dose-response information has often been lacking. We have reexamined the ability of one such compound-caffeine-to induce SCEs and also to inhibit cellular proliferation in human peripheral lymphocytes in vitro. An acute exposure to caffeine prior to the DNA synthetic period did not affect either SCE frequency or the rate of cellular proliferation. Chronic exposure to caffeine throughout the culture period lead to both a dose-dependent increase in SCEs (SCEd or doubling dose = 2.4 mM; SCE10 or the dose capable of inducing 10 SCE = 1.4 mM) and a dose-dependent inhibition of cellular proliferation (IC50 or the 50% inhibition concentration = 2.6 mM). The relative proportion of first generation metaphase cels, an assessment of proliferative inhibition, increased linearly with increasing caffeine concentrations. However, SCE frequency increased nonlinearly over the same range of caffeine concentrations. Examination of the ratio of nonsymmetrical to symmetrical SCEs in third generation metaphase cells indicated that caffeine induced SCEs in equal frequency in each of three successive generations. The dependency of SCE induction and cellular proliferative inhibition on caffeine's presence during the DNa synthetic period suggests that caffeine may act as an antimetabolite in normal human cells. The significance of these results in regard to both caffeine's genotoxic potential and to the reliability of the SCE assay system are discussed.

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Chromosome Aberrations Induced in Cultured Human Cells by Caffeine

Abstract: Caffeine (1, 3, 7-trimethylxanthine) is suspect as a possible mutagen because of its purine nature.In view of our frequent contact with it in relatively large quantities in soft drinks, tea, and coffee, as well as in drugs, its possible mutagenicity presents a serious

Cited by 28 publications

References 16 publications

Growth and death of hela cells in the presence of caffeine

Growth and death of hela cells in the presence of caffeine

Effect on the Offspring of Repeated Caffeine Administration to Pregnant Rats

Induction of sister chromatid exchanges and inhibition of cellular proliferation in vitro. I. caffeine

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