Repair of UV damaged DNA in systemic lupus erythematosus.
The NZB/NZW hybrid mouse is an animal model of human systemic lupus erythematosus (SLE). Two breeding schemes were devised using NZB, NZW, B/W, and CBA mice, which permit definitive decisions regarding genetic and/or viral origin of the disease. It is proposed that at least two factors must be involved: (1) a genetic abnormality producing hyper-responsiveness to nucleic acid antigens, and (2) a DNA repair defect which results in liberation of DNA and RNA when cells are lethally injured. Evidence is presented for a DNA repair deficit in human SLE lymphocytes following in vitro irradiation with ultraviolet (UV) light. Lymphocytes from adult New Zealand and control mice were found to lack normal amounts of endonuclease necessary for repairing UV damage.
D000328:Adult; D000818:Animals; D001345:Autoradiography; D001947:Breeding; D001973:Bromodeoxyuridine; D004247:DNA / Q000528:radiation effects*; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000528:radiation effects; D005799:Genes, Dominant; D005808:Genes, Recessive; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000235:genetics* / Q000382:microbiology; D008214:Lymphocytes / Q000528:radiation effects; D008264:Macrophages / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008815:Mice, Inbred Strains; D011832:Radiation Injuries; D013154:Spleen / Q000166:cytology; D013936:Thymidine / Q000378:metabolism; D014466:Ultraviolet Rays
D004247:DNA; D001973:Bromodeoxyuridine; D013936:Thymidine