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1973年Jones氏首先报道了胎儿酒精中毒症候群。继之许多临床和实验研究表明,妊娠时酒精的慢性接触能使胎儿畸形数显著增加,主要有颅面畸形、心脏缺损、四肢畸形、中枢神经系统异常、尿生殖器官畸形和产前生长的缺陷。酒精接触引起胎儿有害反应的最低水平尚未测定,某些报告提出妊娠时母亲甚至饮用中等水平的酒精就可能造成胎儿发育的紊乱。酒精对胚胎发育的作用方式还不了解,而且它对子宫内胚胎的染色体是否有改变,以前还没有报道过。SCE(姊妹染色单体互换)的频率曾被用来作为致突变和致癌的灵敏指标。已经证明许多致突变物质,在不引起肉眼可见的染色体畸变的浓度时,即可引起SCE的升高。Perry氏用22种已知的致突变剂和致癌剂证明SCE频率增加一倍,但此剂量仅引起
In 1973, Jones first reported fetal alcohol syndrome. Following many clinical and experimental studies have shown that chronic alcohol exposure during pregnancy can significantly increase the number of fetal malformations, there are mainly craniofacial deformity, heart defects, limb deformities, central nervous system abnormalities, genitourinary malformations and prenatal growth defects . The minimum level of harmful fetal exposure to alcohol exposure has not been determined, and some reports suggest that mothers may even develop moderate levels of alcohol during pregnancy that may cause fetal development disorders. The mode of action of alcohol on embryonic development is unknown, and it has not been reported before on the chromosome of the uterine embryo. The frequency of SCE (sister chromatid exchange) has been used as a sensitive indicator of mutagenicity and carcinogenesis. Many mutagenic substances have been shown to cause an increase in SCE at concentrations that do not cause macroscopic chromosomal aberrations. Perry’s use of 22 known mutagens and carcinogens demonstrated a doubling of the SCE frequency but only caused this dose