Published October 1966 | Version v1
Book

Processes Underlying Repair and Radiosensitivity in Spermatozoa and Spermatids of Drosophila

  • 1. Department of Radiation Genetics, University of Leiden (Netherlands)

Description

When Drosophila males are exposed to X-irradiation under anoxia, and the effects of post-treatment with N2 are compared with those with O2, a reduction of the mutation- and translocation frequencies is observed with N2 in spermatozoa, but with O2 in early spermatids. Since the same results have now been obtained with spermatozoa treated in inseminated females, and with spermatids from 24-h- old pupae, these post-radiation modifications cannot be from errors in the sampling of germ cells with different radiosensitivities. Experimental evidence suggests that In both types of cells, the post-radiation effects arise from enzymatic repair of potential lesions leading to mutation or chromosome breaks. For sperm it could be demonstrated that neither post-radiation interaction of radicals with O2, nor selective elimination of cells with genetic damage by post-treatment with N2 can explain the observed effects. Radiosensitization after pre-treatment with sodium fluoride, iodoacetamide, ribonuclease or actinomycin-D suggests that in sperm both glycolytic enzymes and RNA or protein synthesis are involved in the repair process. In the early spermatids, on the other hand, oxygen is clearly required for repair to occur, and inhibition of RNA and/or protein synthesis by pre-treatment with actinomycin-D, ribonuclease or chloramphenicol leads to a reduction of the radiation-induced mutation frequency. Studies on the origin of stage-specific differences in radiosensitivity showed that early spermatids are characterized by a considerably higher oxygen enhancement ratio than spermatozoa. Their greater response to radiation as compared with sperm thus arises from a greater intrinsic sensitivity to the induction of radiation damage in the presence of O2. Oxygen enhancement ratios for folly mature spermatozoa and late spermatids, however, do not differ significantly, but the higher radiosensitivity in the former than in the latter cells appears to originate from a greater degree of oxygenation, under normal conditions in air. (author)

Part of:
Genetical Aspects of Radiosensitivity: Mechanisms of Repair. Proceedings of a Panel

Additional details

Publishing Information

Publisher
IAEA
Imprint Place
Vienna (International Atomic Energy Agency (IAEA))
Imprint Title
Genetical Aspects of Radiosensitivity: Mechanisms of Repair. Proceedings of a Panel
Imprint Pagination
178 p.
Series
Panel Proceedings Series
Journal Page Range
p. 49-64
ISSN
0074-1876

Conference

Title
Mechanisms of Repair
Acronym
Panel on Genetical Aspects of Radiosensitivity
Dates
18-22 Apr 1966
Place
Vienna (Austria)

Optional Information

Contract/Grant/Project number
Contract 052-64-1 BIAN
Notes
30 refs., 11 figs.
Secondary number(s)
STI-PUB--130