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a School of Biological Sciences, University of Manchester, Manchester M13 9PT, United Kingdom
b CRC Experimental Radiation Oncology Group Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester M20 4BX, United Kingdom
c Genetics Unit, Westlakes Research Institute, Moor Row, Cumbria CA24 3JY, United Kingdom
The single-cell gel electrophoresis (Comet) assay has been widely used to measure DNA damage in human sperm in a variety of physiological and pathological conditions. We investigated the effects of in vivo radiation, a known genotoxin, on spermatogenic cells of the mouse testis and examined sperm collected from the vas deferens using the neutral Comet assay. Irradiation of differentiating spermatogonia with 0.25–4 Gy X-rays produced a dose-related increase in DNA damage in sperm collected 45 days later. Increases were found when measuring Comet tail length and percentage of tail DNA, but the greatest changes were in tail moment (a product of tail length and tail DNA). Spermatids, spermatocytes, differentiating spermatogonia, and stem cell spermatogonia were also irradiated in vivo with 4 Gy X-rays. DNA damage was indirectly deduced to occur at all stages. The maximum increase was seen in differentiating spermatogonia. DNA damaged cells were, surprisingly, still detected 120 days after stem cell spermatogonia had been irradiated. The distribution of DNA damage among individual sperm cells after irradiation was heterogeneous. This was seen most clearly when changes in the Comet tail length were measured when there were discrete undamaged and damaged populations. After increasing doses of irradiation, an increasing proportion of cells were found in the damaged population. Because a proportion of undamaged sperm cells remains after all but the highest dose, the possibility of normal fertility remains. However, fertilization with a spermatozoa carrying high amounts of DNA damage could lead to effects as diverse as embryonic death and cancer susceptibility in the offspring.
1 G.H. was supported by United Kingdom BBSRC. J.H. was supported by the United Kingdom CRC.
2 Correspondence: I.D. Morris, School of Biological Sciences, G38 Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, U.K. FAX: 0161 275 5600; i.morris{at}man.ac.uk
3 Current address: Department of Genetic Toxicology, Huntingdon Life Sciences, Eye Research Centre, Suffolk PE28 4HS, U.K
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