DeSesso J M
Teratog Carcinog Mutagen. 1987;7(3):225-40. doi: 10.1002/tcm.1770070305.
The maternal organism provides the developing embryo with its physical environment, nutrients, and a mechanism for eliminating metabolic wastes. Since the physiological state of the pregnant female affects her ability to provide those requirements for the developing embryo, it is not surprising that there are maternal factors that can affect the wellbeing of the embryo. Extremes of maternal age in both humans and animals have been implicated in growth retardation, as well as autosomal trisomies. The influence of maternal size on fetal size is more pronounced among larger species with longer gestation periods such as humans and domestic animals. A clear relationship between the parity of the mother and potential developmental toxicity in humans has not been established due to the confounding influences of maternal age. Among laboratory rodents, however, it appears that offspring of multiparous animals are at increased risk of developmental toxicity. A variety of infectious agents, particularly viruses, have either been demonstrated or implicated as causes of developmental toxicity. In addition, hyperthermia is a possible confounding factor inherent with maternal infection. Although under experimental conditions hyperthermia is teratogenic in laboratory animals, a causative role for transient hyperthermia, which occurs during febrile states concomitant with infections, cannot be clearly established. Chronic maternal vascular disease states including essential hypertension, heart disease, or diabetes mellitus are likely to contribute to uteroplacental insufficiency and developmental toxicity. Poor maternal nutrition among humans contributes to growth retardation, but not to malformations. The production of "abnormal" maternal antibodies, such as are present in Rh incompatibility, can cause fetal wastage. An important maternal factor in humans is uteroplacental insufficiency, which can occur in normal states like twinning, as well as in abnormal conditions including reduced placental size, chronic maternal hypoxia, or uterine ischemia. Although all these maternal factors can contribute to developmental toxicity, they do not necessarily occur as isolated events. Some developmental toxicants exert deleterious effects within both the embryo and the maternal system.
母体为发育中的胚胎提供其物理环境、营养物质以及清除代谢废物的机制。由于怀孕女性的生理状态会影响她为发育中的胚胎提供这些需求的能力，因此存在能够影响胚胎健康的母体因素也就不足为奇了。人类和动物母体年龄的极端情况都与生长迟缓以及常染色体三体性有关。在人类和家畜等妊娠期较长的较大物种中，母体大小对胎儿大小的影响更为明显。由于母体年龄的混杂影响，尚未确定母亲的生育次数与人类潜在发育毒性之间的明确关系。然而，在实验啮齿动物中，似乎多胎动物的后代发育毒性风险增加。多种传染因子，尤其是病毒，已被证实或被认为是发育毒性的原因。此外，体温过高是母体感染所固有的一个可能的混杂因素。尽管在实验条件下体温过高在实验动物中具有致畸性，但对于发热状态伴随感染时发生的短暂体温过高的致病作用尚无法明确确定。慢性母体血管疾病状态，包括原发性高血压、心脏病或糖尿病，很可能导致子宫胎盘功能不全和发育毒性。人类母体营养不良会导致生长迟缓，但不会导致畸形。“异常”母体抗体的产生，如存在于Rh血型不相容中的抗体，可导致胎儿死亡。人类中一个重要的母体因素是子宫胎盘功能不全，它可发生在双胎妊娠等正常状态下，也可发生在胎盘尺寸减小、母体慢性缺氧或子宫缺血等异常情况下。尽管所有这些母体因素都可能导致发育毒性，但它们不一定是孤立发生的。一些发育毒物会在胚胎和母体系统内都产生有害影响。
