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In vitro Repair of Oxidative DNA Damage by Human Nucleotide Excision Repair System: Possible Explanation for Neurodegeneration in Xeroderma Pigmentosum Patients
Joyce T. Reardon, Tadayoshi Bessho, Hsiang Chuan Kung, Philip H. Bolton and Aziz Sancar
Proceedings of the National Academy of Sciences of the United States of America
Vol. 94, No. 17 (Aug. 19, 1997), pp. 9463-9468
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/42627
Page Count: 6
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Xeroderma pigmentosum (XP) patients fail to remove pyrimidine dimers caused by sunlight and, as a consequence, develop multiple cancers in areas exposed to light. The second most common sign, present in 20-30% of XP patients, is a set of neurological abnormalities caused by neuronal death in the central and peripheral nervous systems. Neural tissue is shielded from sunlight-induced DNA damage, so the cause of neurodegeneration in XP patients remains unexplained. In this study, we show that two major oxidative DNA lesions, 8-oxoguanine and thymine glycol, are excised from DNA in vitro by the same enzyme system responsible for removing pyrimidine dimers and other bulky DNA adducts. Our results suggest that XP neurological disease may be caused by defective repair of lesions that are produced in nerve cells by reactive oxygen species generated as by-products of an active oxidative metabolism.
Proceedings of the National Academy of Sciences of the United States of America © 1997 National Academy of Sciences