Abstract：
:Xeroderma pigmentosum (XP) is a genetic disorder associated with defects in nucleotide excision repair, a pathway that eliminates a wide variety of helix-distorting DNA lesions, including ultraviolet-induced pyrimidine dimers. In addition to skin diseases in sun-exposed areas, approximately 25% of XP patients develop progressive neurological disease, which has been hypothesized to be associated with the accumulation of an oxidatively generated type of DNA damage called purine 8,5'-cyclo-2'-deoxynucleoside (cyclopurine). However, that hypothesis has not been verified. In this study, we tested that hypothesis by using the XP group A gene-knockout (Xpa-/-) mouse model. To quantify cyclopurine lesions in this model, we previously established an enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody (CdA-1) that specifically recognizes 8,5'-cyclo-2'-deoxyadenosine (cyclo-dA). By optimizing conditions, we increased the ELISA sensitivity to a detection limit of ˜one cyclo-dA lesion/106 nucleosides. The improved ELISA revealed that cyclo-dA lesions accumulate with age in the brain tissues of Xpa-/- and of wild-type (wt) mice, but there were significantly more cyclo-dA lesions in Xpa-/- mice than in wt mice at 6, 24 and 29 months of age. These findings are consistent with the long-standing hypothesis that the age-dependent accumulation of endogenous cyclopurine lesions in the brain may be critical for XP neurological abnormalities.
journal_name
DNA Repair (Amst)journal_title
DNA repairauthors
Mori T,Nakane H,Iwamoto T,Krokidis MG,Chatgilialoglu C,Tanaka K,Kaidoh T,Hasegawa M,Sugiura Sdoi
10.1016/j.dnarep.2019.04.004subject
Has Abstractpub_date
2019-08-01 00:00:00pages
52-58eissn
1568-7864issn
1568-7856pii
S1568-7864(19)30005-9journal_volume
80pub_type
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