scholarly journals Mutagenicity of DDT in Mice, Drosophila melanogaster and Neurospora crassa

1974 ◽  
Vol 27 (4) ◽  
pp. 427 ◽  
Author(s):  
Julian M Clark
Keyword(s):  
Body Weight ◽  
Acute Treatment ◽  
Chromosome Breakage ◽  
Male Mice ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Dominant Lethal Mutations ◽  
Early Spermatid ◽  
Dominant Lethal Assay ◽  
Oral Doses

The pesticide DDT was examined for possible mutagenicity in mice, D. melanogaster and N. crassa. Through the use of the dominant-lethal assay it was found that acute oral doses of DDT (2 x 150 mg/kg body weight) in male mice induced dominant lethal mutations in early spermatid and spermato-cyte stages. Chronic oral doses of DDT (2 x 100 mg/kg body weight per week for 10 weeks) in male mice caused a persistent increase in the number of dominant lethal mutations. Histological sections showed that chronic treatment of mice with DDT caused changes in seminiferous tubule morphology and degeneration of B-type spermatogonia. Acute treatment of mice with DDT caused an increase in spermatocyte chromosome breakage, stickiness and precocious separation of the X and Y bivalent.

scholarly journals EFFECTS OF DOSE ON THE INDUCTION OF DOMINANT-LETHAL MUTATIONS AND HERITABLE TRANSLOCATIONS WITH ETHYL METHANESULFONATE IN MALE MICE

Genetics ◽  
1974 ◽  
Vol 77 (4) ◽  
pp. 741-752
Author(s):  
W M Generoso ◽  
W L Russell ◽  
Sandra W Huff ◽  
Sandra K Stout ◽  
D G Gosslee
Keyword(s):  
Dose Response ◽  
Response Curve ◽  
Chromosome Breakage ◽  
Ethyl Methanesulfonate ◽  
Dose Response Curve ◽  
Male Mice ◽  
Lethal Mutations ◽  
Dominant Lethal ◽  
Dominant Lethal Mutations ◽  
Dominant Lethals

ABSTRACT Genetic damage by ethyl methanesulfonate (EMS) in male mice was measured at doses ranging from 50 to 300 mg/kg with dominant-lethal mutations and reciprocal translocations as endpoints. No appreciable increase in dominant-lethal mutations was detected following a dose of 100 mg/kg. Dominant lethals induced by EMS were convincingly detected only after a dose of 150 mg/kg, but in the translocation experiment an increase in the genetic effect was detectable at the 50 mg/kg dose. It is likely that dominant lethals had also been induced at the 50 and 100 mg/kg doses, but were not detected due to the relative insensitivity of the dominant%lethal procedure. Thus, for detection of low levels of EMS-induced chromosome breakage, translocations are a much more reliable endpoint than are dominant-lethal mutations. A procedure for large-scale screening of induced translocations is described.—The dominant-lethal dose-response curve, plotted on the basis of living embryos as a percentage of the control value, is clearly not linear as it is markedly concave downward. Similarly, the translocation dose-response curve showed a more rapid increase in the number of translocations with dose than would be expected on the basis of dose-square kinetics. It is clear for both of these endpoints that the effectiveness of EMS in inducing chromosome breakage is proportionately much lower at low doses.

scholarly journals Dominant lethal mutations induced in male mice by methyl methanesulphonate

Heredity ◽  
1964 ◽  
Vol 19 (2) ◽  
pp. 191-200 ◽  
Author(s):  
M Partington ◽  
A J Bateman
Keyword(s):  
Male Mice ◽  
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.

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