Germ-cell sensitivity in mammals.
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.
D000818:Animals; D002869:Chromosome Aberrations; D005260:Female; D005854:Germ Cells / Q000187:drug effects*; D006801:Humans; D008297:Male; D051379:Mice; D009153:Mutagens / Q000494:pharmacology; D009865:Oocytes / Q000187:drug effects; D013094:Spermatozoa / Q000187:drug effects / Q000528:radiation effects / Q000648:ultrastructure
D009153:Mutagens