title: How do male germ cells handle DNA damage?
abstract: Male reproductive health has received considerable attention in recent years. In addition to declining sperm quality, fertility problems and increased incidence of testicular cancer, there is accumulating evidence that genetic damage, in the form of unrepaired DNA lesions or de novo mutations, may be transmitted via sperm to the offspring. Such genetic damage may arise from environmental exposure or via endogenously formed reactive species, in stem cells or during spermatogenesis. Damaged testicular cells not removed by apoptosis rely on DNA repair for their genomic integrity to be preserved. To identify factors with potentially harmful effects on testicular cells and to characterise associated risk, a thorough understanding of repair mechanisms in these cells is of particular importance. Based on results from our own and other laboratories, we discuss the current knowledge of different pathways of excision repair in rodent and human testicular cells. It has become evident that, in human spermatogenic cells, some repair functions are indeed non-functional.
authors.affiliation: Norwegian Institute of Public Health, Department of Chemical Toxicology, P.O. Box 4404 Nydalen, N-0403 Oslo, Norway.
authors.forename: Ann-Karin
authors.initials: AK
authors.lastname: Olsen
authors.forename: Birgitte
authors.initials: B
authors.lastname: Lindeman
authors.forename: Richard
authors.initials: R
authors.lastname: Wiger
authors.forename: Nur
authors.initials: N
authors.lastname: Duale
authors.forename: Gunnar
authors.initials: G
authors.lastname: Brunborg
mesh_terms: D000818:Animals; D004249:DNA Damage; D004260:DNA Repair; D005298:Fertility / Q000187:drug effects; D006801:Humans; D008297:Male; D012098:Reproduction / Q000187:drug effects; D013091:Spermatogenesis / Q000187:drug effects; D013094:Spermatozoa / Q000187:drug effects* / Q000648:ultrastructure