Chemical induction of presumed dominant-lethal mutations in postcopulation germ cells of mice. I. Relative sensitivity between pre- and postcopulation germ cells to isopropyl methanesulfonate

1975 ◽  
Vol 30 (3) ◽  
pp. 355-363 ◽  
Author(s):  
Kurt E. Suter
Keyword(s):  
Germ Cells ◽  
Relative Sensitivity ◽  
Chemical Induction ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Dominant Lethal Mutations

scholarly journals Induction of specific-locus and dominant lethal mutations in male mice by ifosfamide (Holoxan)

1998 ◽  
Vol 72 (3) ◽  
pp. 177-183 ◽  
Author(s):  
U. H. EHLING ◽  
J. FAVOR ◽  
A. NEUHÄUSER-KLAUS ◽  
I.-D. ADLER
Keyword(s):  
Germ Cell ◽  
Germ Cells ◽  
Genetic Risk ◽  
Male Mice ◽  
Induced Mutations ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Cell Specificity ◽  
Dominant Lethal Mutations ◽  
Specific Locus

Ifosfamide induced dominant lethal mutations in spermatozoa of mice at doses of 200 and 300 mg/kg and in spermatids and spermatocytes at 600 mg/kg. The highest dose also induced specific-locus mutations in post-spermatogonial germ-cell stages of mice but not in spermatogonial stem cells. The nature of the induced mutations suggests they are intergenic. The spermatogenic specificity of ifosfamide in mouse germ cells is similar to that of the structurally related cytostatic drugs cyclophosphamide and trofosfamide. Due to the post-spermatogonial germ cell specificity of ifosfamide, the genetic risk is limited to a few weeks after exposure.

scholarly journals RELATIVE RATES AT WHICH DOMINANT-LETHAL MUTATIONS AND HERITABLE TRANSLOCATIONS ARE INDUCED BY ALKYLATING CHEMICALS IN POSTMEIOTIC MALE GERM CELLS OF MICE

Genetics ◽  
1979 ◽  
Vol 93 (1) ◽  
pp. 163-171
Author(s):  
Walderico M Generoso ◽  
Sandra W Huff ◽  
Katherine T Cain
Keyword(s):  
Dna Synthesis ◽  
Germ Cells ◽  
Chromosomal Aberrations ◽  
The Other ◽  
Male Germ Cells ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Dominant Lethal Mutations ◽  
Close Relationship ◽  
Repair Activity

ABSTRACT There is a close relationship between the rates at which dominant lethal mutations and heritable translocations are induced by ethyl methanesulfonate (EMS) or triethylenemelamine (TEM) in male postmeiotic germ cells. This relationship does not hold for isopropyl methanesulfonate (IMS), which induced only negligible frequencies of heritable translocations at doses that induced high levels of dominant lethal mutations. Nor does IMS behave like EMS and TEM in the degree to which eggs of different stocks of females repair premutational lesions that are carried in the sperm—large differences between stocks for IMS treatment and small differences for EMS or TEM treatment. These dissimilarities between IMS and the other two alkylating chemicals are postulated to be attributable to differences in the types of lesions present at the time of repair activity and to whether or not chromosomal aberrations are already fixed prior to postfertilization pronuclear DNA synthesis.

scholarly journals EFFECTS OF DOSE ON THE INDUCTION OF DOMINANT-LETHAL MUTATIONS WITH TRIETHYLENEMELAMINE IN MALE MICE

Genetics ◽  
1974 ◽  
Vol 77 (4) ◽  
pp. 753-763
Author(s):  
B E Matter ◽  
W M Generoso
Keyword(s):  
Lethal Dose ◽  
Dose Effect ◽  
Chemical Induction ◽  
Response Curves ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Dominant Lethal Mutations ◽  
Two Stages ◽  
Mutagenic Effects

ABSTRACT Dose effects of triethylenemelamine (TEM) in the induction of dominant-lethal mutations were studied at the early spermatozoon, midspermatid and spermatocyte stages. The pattern of effects on spermatocytes, unlike midspermatids and early spermatozoa, indicated possible cytotoxic damage, so for the determination of TEM dose-response curves in the induction of genetic damage only the data for midspermatids and early spermatozoa were used. The TEM dose-effect curves for those two stages differ markedly from ethyl methanesulfonate (EMS) dose-effect curves. Beginning with the lowest doses at which significant effects are observed, there is a considerably more rapid increase in dominant-lethal effects with dose of EMS than TEM. Another marked difference between the two compounds is in the ratio of the genetically effective dose (as measured by dominant-lethal mutations) to the lethal dose. The ratio is 1:100 for TEM and only 1:3.5 for EMS; thus, TEM is mutagenic far below its toxic level. Obviously, these results have important implications not only for our understanding of the nature of chemical induction and recovery of chromosomal aberrations but also for the practical problems of evaluating the mutagenic effects of chemicals.

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