アルコール投与マウスのF1胎仔における染色体異常発生

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  • Cytogenetic effects of maternal alcohol uptake on F1 mouse fetuses.
  • アルコール投与マウスのF1胎仔における染色体異常発生〔英文〕
  • アルコール トウヨ マウス ノ F1タイシ ニ オケル センショクタイ イジョ

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Yamamoto et al. (1982)1) attempted cytogenetic analysis of artificial abortion cases in the first trimester before clinical spontaneous abortion in order to elucidate the mechanism of appearance of chromosome anomalies. The factors studied were the presence of diseases, X-ray therapy, medication, smoking and alcohol drinking. However, statistical analysis could be performed mainly for X-ray therapy and medication alone, because the number of patients exposed to any other factor was too small.<BR>In such an epidemiological study, analysis of factors involved in the appearance of chromosome anomalies is difficult, especially when tests for significance can not be done adequately because the frequency of an anomaly is low or the number of subjects exposed to a certain factor is small. The present study was carried out using an animal model to investigate the cytogenetic effects of maternal alcohol ingestion which has been difficult to analyze in the epidemiological study in humans.<BR>The following studies have been made thus far on the effects of ethyl alcohol (abbreviated to alcohol in this paper) on fetuses.<BR>Ulleland (1972)2) reported one possibility of cause-and-effect relationship between mothers as habitual drinkers and low body-weight neonatus with retarded growth and development. Jones et al. (1973)3, 4) paid attention to the presence of several fetuses with characteristic anomalies from habitual alcohol drinking mothers and called them "fetal alcohol syndrome", emphasizing the relationship between alcohol ingestion and anomalies. Since then, several other similar reports have been advanced. In addition, teratogenicity of alcohol ingestion has as yet not been sufficiently elucidated. There are also many reports on the relationship between alcohol ingestion and chromosome anomalies. Rieger and Michaelis (1967)5) reported that chromosome anomalies which were the same as those induced by the alkylating agent, a representative mutagen, were noted when the root cap cells of vicia fava were exposed to alcohol. Bregman (1971)6) noted that the number of chromatid-type chromosome anomalies increased when human lymphocytes were added to 1.2% alcohol and cultured for 4 or 48 hours. It has also been reported that the frequency of sister chromatid exchange (SCE) increased as a result of addition of alcohol or acetaldehyde7, 8) and that of chromosome anomalies was elevated in peripheral lymphocytes of alcoholics9, 10). However, there are only a few reports on the appearance of chromosome anomalies in children from habitual alcohol drinking mothers. Accordingly, the persent study was carried out using an animal model to elucidate the cytogenetic effects of maternal alcohol ingestion on fetuses, especially the appearance of anomalies such as trisomy and monosomy and the possibility of other structural chromosome anomalies.

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