ABSTRACT
Intraperitoneal administration of 500 mg/kg and 625 mg/kg doses of the germ cell mutagen, ethyl methanesulphonate (EMS) in 5 consecutive days to the house rat, Rattus rattus caused a dose-dependent reduction in its body weight, cauda epididymides weight, concentration, motility and percentage of live spermatozoa with simultaneous increase in the percentage of their abnormal forms. Compared to 0·65% spermatozoa with abnormal heads in the cauda epididymidis of untreated control rats, 24·86% and 65·72% such spermatozoa were observed in rats on day 14 post treatment with 500 mg/kg and 625 mg/kg doses of EMS respectively. On day 28 post treatment corresponding values for abnormal spermatozoa were 16·21% and 14·32%. Similarly, spermatozoa with abnormal flagella increased from 0·78% in control rats to 9·25% and 5·75% on day 14 post treatment of 500 and 625 mg/kg doses of EMS respectively and declined to 2·91% and 2·40% on day 28 post treatment. Abnormality in the sperm head was mainly due to acrosomelessness and in the flagellum due to bending at proximal region. However, the main effect of EMS was the development of spermatozoa without or deformed acrosomes which may impair the fertility of rats. Analysis of various stages of differentiation of spermatozoa inthe testis revealed that population of preleptotene and pachytene spermatocytes and of round spermatids showed a gradual decline which became significantly less than controls on day 28 of EMS treatment. Occurrence of abnormal heads of testicular spermatids indicated that the sperm head abnormalities originated in the testis during late spermiogenesis.
ABSTRACT
The cell survival rate and the chromosomal aberration induced by N-methyl-N-nitro-N-nitriosoguanidine (MNNG), mitomycin C (MMC) and ethyl methanesuiphonate (EMS) in V79 cells and its ?-ray-sensitive mutants (irs5 and mil) were observed in this study. The concentrations of mutagens to determine the survival rate were arranged at 2.5~ 30 ?mol/L in MNNG, 1~20?mol/L in MMC and 2~ 16 ?mol/L in EMS, respectively. The cell survival rates and the cell clones of irs5 were higher than that of the V79 cells and irs11; and of irs11 were significantly lower than that of V79 cells and irs5. The result of IC50 of mutagens to determine the chromosomal aberration was similar to the cell survival rate. The type and frequency of chromosomal aberration induced by MNNG, MMC and EMS in irs5 was same as in V79 cell; and there was a dose-response relationship between them. The spontaneous aberration frequencies in irsS and V79 cells were lower than 4%, however, in irs11 was higher than 10%. Data suggests that the cellular biological characterization in irs5 is steady, and further study to certain irsS whether it will be a new mutant for the mutagenicity or carcinogenicity assay or not.