Adler I D
Prog Clin Biol Res. 1982;109:137-48.
The differences in mammalian germ-cell sensitivity have been studied with a number of mutagenic agents using both chromosomal aberrations and point mutations as genetic endpoints. I have tried to give a survey on the present knowledge. Several conclusions can be drawn at present: 1. In spermatogenesis the sensitivity to mutation induction differs between various post-spermatogonial stages and spermatogonia. 2. Heritable structural chromosomal changes are primarily recovered from post-spermatogonial germ cells. The sensitivity pattern is similar in dominant lethal and heritable translocation experiments. The effect recovered from spermatogonia is near zero. 3. Structurally related chemicals show a difference in their spermatogenic response. The most obvious example gave the induction of specific locus mutations by ENU and MNU. 4. Since too little information is available it seems prudent to assume that oocytes and spermatogonia may show similar sensitivity so that in risk estimates effects on female germ cells cannot be neglected. The final result from the previous discussion must be that the limitations of knowledge are obvious, they lie in the limited number of chemicals tested in mammalian germ-cell assays. A larger data base of mammalian germ-cell response to chemical mutagens is urgently needed.
利用多种诱变剂,以染色体畸变和点突变作为遗传终点,对哺乳动物生殖细胞的敏感性差异进行了研究。我试图对目前的知识进行综述。目前可以得出几个结论:1. 在精子发生过程中,精原细胞后期的各个阶段与精原细胞对突变诱导的敏感性不同。2. 可遗传的染色体结构变化主要来自精原细胞后期的生殖细胞。在显性致死和可遗传易位实验中,敏感性模式相似。从精原细胞中恢复的效应接近零。3. 结构相关的化学物质在生精反应上存在差异。最明显的例子是ENU和MNU诱导特定基因座突变。4. 由于可用信息太少,谨慎的做法似乎是假定卵母细胞和精原细胞可能表现出相似的敏感性,因此在风险评估中,对雌性生殖细胞的影响不能被忽视。先前讨论的最终结果必然是,知识的局限性显而易见,它们这些这些这些局限性在于在哺乳动物生殖细胞试验中测试的化学物质数量有限。迫切需要一个关于哺乳动物生殖细胞对化学诱变剂反应的更大的数据库。