| Abstract: | Sex-linked recessive lethal mutations were induced in D melanogaster males by chronic as well as acute treatments of gaseous 1, 2-dibromoethane ranging from 2.3 to 31 ppm.hr. Acute treatments corresponding to each chronic treatment were made by increasing chemical concentration approximately 30 times with a concomittant decrease in exposure period. Germ cell stages sampled, in order of decreasing sensitivity, were spermatocytes, spermatids, and spermatozoa. The most significant finding is that no consistent pattern of difference is observed between acute and chronic exposure for three of the four exposure levels. Only at the highest exposure level (30–31 ppm.hr) was any consistent difference observed between chronic and acute exposure levels. At the higher exposure level in all three germ cell stages the acute exposure showed a significant increase in mutation frequency over the chronic exposure. The greater acute vs chronic mutation frequency for spermatozoa, a metabolically inactive cell stage, leads to the conclusion that the exposure rate effect at high exposure levels is due to systemic factors such as metabolic deactivation or elimination rather than repair of premutational damage in the target cells. The significance of these observations in risk assessment for environmental pollutants is discussed. |
