Abstract
Repair replication and rejoining of single-strand breaks after X-irradiation in human-skin fibroblasts from normal donors and several patients with xeroderma pigmentosum have been compared. The xeroderma strains showed different levels of repair replication following UV exposure. Repair replication and rejoining of breaks, which are considered to be part of the repair mechanism after damage due to X-irradiation and UV-irradiation, appeared to be performed in all xeroderma pigmentosum strains tested to the same level as in control strains. These results, and the observation that in the same xeroderma pigmentosum strains repair replication after UV irradiation was considerably reduced, suggest that the xeroderma strains investigated were deficient in the enzyme(s) involved in the excision of pyrimidine dimers from the DNA.
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