Kale P G, Baum J W
Environ Mutagen. 1981;3(1):65-70. doi: 10.1002/em.2860030107.
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 concomitant 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.
通过对气态1,2 - 二溴乙烷进行2.3至31 ppm·小时范围内的慢性和急性处理，在黑腹果蝇雄性中诱导出性连锁隐性致死突变。对应于每种慢性处理的急性处理是通过将化学物质浓度提高约30倍并同时缩短暴露时间来进行的。按敏感性递减顺序采样的生殖细胞阶段为精母细胞、精子细胞和精子。最显著的发现是，在四个暴露水平中的三个水平上，急性暴露和慢性暴露之间未观察到一致的差异模式。仅在最高暴露水平（30 - 31 ppm·小时）下，慢性暴露水平和急性暴露水平之间观察到任何一致的差异。在所有三个生殖细胞阶段的较高暴露水平下，急性暴露的突变频率相对于慢性暴露显著增加。精子细胞是代谢不活跃的细胞阶段，其急性突变频率相对于慢性突变频率更高，这导致得出结论：高暴露水平下的暴露率效应是由于全身因素，如代谢失活或消除，而不是靶细胞中预突变损伤的修复。讨论了这些观察结果在环境污染物风险评估中的意义。
