Yielding K L
University of Texas Medical Branch, Galveston.
Environ Health Perspect. 1993 Oct;101 Suppl 3(Suppl 3):285-90. doi: 10.1289/ehp.93101s3285.
Birth defects may be inherited in the germ line or may result primarily from a wide spectrum of predictable physical, chemical, and infectious processes that can operate in the mother, the father, or in the zygote. The systematic consideration of these mechanisms can lead to a fresh awareness of risk and possible strategies toward recognizing and avoiding such risks. Birth defects also depend heavily on secondary factors that may even be of greater concern than any single primary insult because they may simultaneously affect the consequences of more than one primary exposure. Under the influence of secondary factors, the frequency, timing, and intensity of developmental deficiencies can be quite varied. It is particularly interesting that expression can be delayed until quite late in life, and deficiencies may occur or be expressed only in response to the appropriate environmental stress or functional demand. Any discussion of teratogenic mechanisms, therefore, is not complete without taking into account the important concept of co-teratogenesis, or the operation of secondary risk mechanisms. The principle of secondary risk or co-teratogenesis has been demonstrated by means of enhancement of radiation-induced terata by the administration of drugs that inhibit DNA repair. An example of late-onset expression of prenatal damage was illustrated with postnatal retinal degeneration occurring after prenatal damage to the developing retina. It is suggested that a systematic consideration of primary and secondary risk mechanisms can lead to a better understanding of the problem of birth defects.
出生缺陷可能在生殖细胞系中遗传,也可能主要由一系列可预测的物理、化学和感染过程导致,这些过程可发生在母亲、父亲或受精卵中。对这些机制进行系统考量能够带来对风险的全新认识,以及识别和避免此类风险的可能策略。出生缺陷还在很大程度上取决于次要因素,这些因素甚至可能比任何单一的主要损害更令人担忧,因为它们可能同时影响多种主要暴露的后果。在次要因素的影响下,发育缺陷的频率、时间和强度可能会有很大差异。特别有趣的是,表达可能会延迟到生命后期,缺陷可能仅在对适当的环境压力或功能需求做出反应时才会出现或表现出来。因此,在不考虑协同致畸作用这一重要概念或次要风险机制的作用的情况下,对致畸机制的任何讨论都是不完整的。次要风险或协同致畸作用的原理已通过给予抑制DNA修复的药物增强辐射诱导的畸形得以证明。产前损伤的迟发性表达的一个例子是发育中的视网膜在产前受损后出现产后视网膜变性。有人认为,对主要和次要风险机制进行系统考量能够更好地理解出生缺陷问题。