Sandor S
Laboratory of Embryology, Center of Hygiene and Public Health Timisoara, Romania.
Acta Biol Hung. 1988;39(4):419-39.
Experimental data are presented with respect to "experimental alcohol blastopathy" performed in our laboratory. As in our interpretation the notion of blastopathy involves both pathological changes during preimplantation development due to previous, preconceptional or preimplantation influences and later, pre- or postnatal effects induced by factors active during the preimplantation period, up to now the following experimental models were applied (on rats and mice): chronic and acute maternal, biparental or paternal ethanol alcoholization; preimplantation treatment with acetaldehyde or disulfiram followed by ethanol administration; acute ethanol intoxication before implantation on the background of chronic maternal ethanol intake; chronic maternal intake of various beverages. The main components of experimental alcohol blastopathy detected (by using a complex control methodology) were: pathological changes during the preimplantation developmental stages (lower mean number of embryos/animal, retardation of development, lowered migration rate of the embryos from the oviduct to the uterus, higher number of pathological morphological features), delayed implantation, disturbances of the early postimplantation development, retarded late foetal and placental growth. The effect of ethanol may be direct (ethanol being detectable in the oviductal and uterine fluid after both acute and chronic alcoholization) or indirect, via changes of the maternal macro- or microenvironment. The increase of the maternal blood acetaldehyde level may contribute to the appearance of alcohol blastopathy. Chronic beer and wine intake and acute intoxication with cognac suggest - up to now - the enhancing effect of beverage congeners. The noxious effect of acute ethanol intoxication superposed to chronic alcoholization is more marked that the separate effect of the two kinds of treatment. The chronic ethanol intake of fertilizing males (in mice) leads, both in the case of treated or untreated females, to lowered fertilization efficiency, to retardation of development (not occurring in the experimental model with chronic alcoholization of females) and to an enhanced increase of the number of pathological features. The cytogenetic control of preimplantation embryos (after chronic, acute or combined treatment with ethanol) does not reveal significant chromosomal changes. A possible alcohol blastopathy in humans must be taken into account (i.e. a noxious effect during the very early period of pregnancy when it is ignored).
本文展示了在我们实验室进行的“实验性酒精胚胎病”的实验数据。在我们的解释中，胚胎病的概念既包括由于先前、孕前或植入前的影响在植入前发育过程中发生的病理变化，也包括由植入前期活跃的因素在后期引起的产前或产后影响。到目前为止，我们应用了以下实验模型（针对大鼠和小鼠）：慢性和急性母体、双亲或父体乙醇酒精化；用乙醛或双硫仑进行植入前处理，随后给予乙醇；在慢性母体摄入乙醇的背景下，植入前急性乙醇中毒；慢性母体摄入各种饮料。（通过使用综合对照方法）检测到的实验性酒精胚胎病的主要成分包括：植入前发育阶段的病理变化（每只动物的胚胎平均数量减少、发育迟缓、胚胎从输卵管向子宫的迁移率降低、病理形态特征数量增加）、植入延迟、植入后早期发育的干扰、晚期胎儿和胎盘生长迟缓。乙醇的作用可能是直接的（急性和慢性酒精化后，在输卵管和子宫液中均可检测到乙醇），也可能是间接的，通过母体宏观或微观环境的变化。母体血液乙醛水平的升高可能导致酒精胚胎病的出现。慢性饮用啤酒和葡萄酒以及急性饮用干邑表明，到目前为止，饮料中的同系物具有增强作用。急性乙醇中毒叠加在慢性酒精化上的有害作用比两种处理单独的作用更为明显。受精雄性（小鼠）慢性摄入乙醇，无论雌性是否接受处理，都会导致受精效率降低、发育迟缓（在雌性慢性酒精化的实验模型中未出现）以及病理特征数量的增加。对植入前胚胎进行细胞遗传学对照（在慢性、急性或乙醇联合处理后）未发现明显的染色体变化。必须考虑人类中可能存在的酒精胚胎病（即在怀孕早期被忽视时产生的有害影响）。
