Comparison of radiation- and chemically-induced dominant lethal mutations in male mice

Abstract

Ionizing radiation-induced dominant lethal mutations in all spermatogenic stages. After irradiation of male mice with 200 R the yield of induced mutations in early spermatids was twice the yield in spermatozoa, late spermatids, and spermatocytes. After irradiation with 400 R or 800 R the spermatocytes were the most sensitive stage for the induction of dominant lethal mutations. The frequency of radiation-induced dominant lethal mutations in postspermatogonial stages was dose-dependent. The yield of dominant lethal mutations in spermatogonia was independent of the dose. Pretreatment with chloramphenicol enhanced the frequency of radiation-induced dominant lethal mutations only in spermatozoa. Pretreatment with S,2-aminoethylisothiuronium · Br · HBr (AET) reduced the frequency of radiation-induced dominant lethal mutations in early spermatids. Chemically mutagens can be characterized by their stage-specific induction of mutations. The straight chain alkyl methanesulfonates ethyl methanesulfonate (EMS), methyl methanesulfonate (MMS) and n-propyl methanesulfonate (PMS) induced a high frequency of dominant lethal mutations in spermatozoa and late spermatids. The induced dominant lethal mutation rate decreased to the control level of embryonic lethality in early spermatids. No mutations were induced in spermatocytes. The absence of induced mutations in spermatozoa and late spermatids was typical for the spermatogenic response after treatment with mytomycin C. Mutations were induced in early spermatids. Spermatocytes were the most sensitive germ-cell stage for the induction of dominant lethal mutations with mitomycin C. Possible explanations for the differential spermatogenic response to radiation- and chemically-induced dominant lethal mutations are discussed.