Repair replication and sister chromatid exchanges as indicators of excisable and nonexcisable damage in human (xeroderma pigmentosum) cells.
Alkylating agents cause damage to DNA which can be repaired by exicsion repair (repair replication) and which induces sister chromatid exhcanges (SCEs). During early times after exposure (within 5 hr) normal and xeroderma pigmentosum (XP) cells perform similar amounts of repair replication. At later times (after 20 hr) normal cells have completed repair replication but XP cells continue at a lower rate. This slowly repaired component of alkylation damage appears to be related to the higher frequencies of SCEs induced by alkylating agents in XP cells compared to normal cells. Therefore, whereas repair replication is an indicator of exicsed damage, SCEs may be indicators of unexcised damage and may show better correlations with the potentially mutagenic and carcinogenic effects of exposure to enbironmental agents.
D000478:Alkylation; D002273:Carcinogens / Q000494:pharmacology; D002460:Cell Line; D002842:Chromatids / Q000502:physiology*; D004247:DNA / Q000378:metabolism / Q000528:radiation effects; D004260:DNA Repair; D004261:DNA Replication; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D013997:Time Factors; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000378:metabolism / Q000503:physiopathology*
D002273:Carcinogens; D004247:DNA