Effect of ethanol on uterotropic action of estrogens

Bershtein, L. M.; Цырлина, Е. В.; Порошина, Т. Е.; Gamayunova, V. B.; Bychkova, N. V.; Калинина, Н. М.; Vasil'ev, D. A.; Коваленко, И. Г.

doi:10.1007/bf02682043

Bull Exp Biol Med

2000

DOI: 10.1007/bf02682043

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Effect of ethanol on uterotropic action of estrogens

L. M. Bershtein

Е. В. Цырлина

Т. Е. Порошина

et al.

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Cited by 2 publications

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“…A large number of epidemiological studies have demonstrated that alcohol and estrogen supplementation act synergistically to increase the risk of breast cancer (Ginsburg 1999). Ethanol ingestion is accompanied by an increase in DNA damage in the uterus induced by estrogen (Bershtein et al 2000). It has been demonstrated that ethanol promotes estrogen-induced prolactinomas and lactotropic proliferation in ovariectomized female rats (De et al 2002).…”

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Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

et al. 2009

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The interaction of chronic alcohol consumption with estrogen has been recognized in various tissues; however, the potential mechanism has not been clearly defined. In this study, we made the following observations: (a) 0.01% (v/v) ethanol (corresponding to 1.7 mM) significantly elevated estrogen receptor alpha (ERalpha) protein content, stimulated activator protein-1 (AP-1)-dependent ERalpha transcriptional activities, and ultimately enhanced GH4C1 cells growth in vitro and (b) the same concentration of ethanol suppressed the stimulatory effects of 17beta-estradiol (E2; 10 nM) on both cell growth and cellular PRL accumulate through attenuation of ERalpha actions at both the estrogen response element and the AP-1 site. These observations raise the question as to what extent ethanol influences signal transduction pathways controlled by E2 in experimental medicine and biology.

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Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

et al. 2009

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The effect of smoking on DNA effects in the comet assay: a meta-analysis

2005

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The comet assay (alkaline single-cell gel electrophoresis, SCG or SCGE) is frequently used in biomonitoring to detect genotoxic effects in humans exposed at the workplace or in their environment. Because of its ready accessibility, blood is most frequently used in such studies. Many studies investigated cigarette smoking either as a genotoxic exposure itself or as a potential confounding factor in occupational studies. However, although smoking is considered to be a relevant exposure towards various genotoxins, conflicting results have been reported in the comet assay studies. The actual reasons for this discrepancy are not known. To further evaluate evidence for smoking-related DNA effects in the comet assay, we now used a meta-analysis approach based on a literature search. We identified 38 studies from 37 publications which were suited for a formal meta-analysis based on the standardized mean difference (SMD) between the study groups. The evaluation of these 38 studies indicated higher levels of DNA damage in smokers than in non-smokers [under a random effects model, SMD = 0.55, 95% confidence interval = (0.16-0.93)]. Subdividing these studies into studies investigating the effect of smoking as a genotoxic exposure (Type A studies, n = 12) and studies investigating smoking as a potential confounder in occupational studies (Type B, n = 26) indicated a significant difference only in Type A studies but not in Type B studies. Furthermore, studies using image analysis or image length measurements (n = 23) only indicated a tendency for a genotoxic effect of smoking, whereas studies using an arbitrary score (n = 15) found a significantly higher level of DNA damage in smokers.

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Effect of ethanol on uterotropic action of estrogens

Cited by 2 publications

References 5 publications

Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

Low-dose ethanol suppresses 17β-estradiol activity in GH4C1 pituitary tumor cells

The effect of smoking on DNA effects in the comet assay: a meta-analysis

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