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Defective Repair of Oxidative Damage in the Mitochondrial DNA of a Xeroderma Pigmentosum Group A Cell Line¹

Department of Structural and Cellular Biology, University of South Alabama, Mobile, Alabama 36688

Recent evidence has linked mitochondrial DNA (mtDNA) damage to several disease processes, including cancer and aging. An important source of such damage is reactive oxygen species. These molecules can be generated endogenously via the electron transport system or may arise from a host of exogenous sources. It has been reported that extracts from cells of individuals with xeroderma pigmentosum group A (XP-A) do not repair some types of oxidative DNA damage. The current experiments were designed to determine whether there is a correlation between the inadequate repair of oxidatively damaged nuclear DNA in XP-A cells and the capacity of such cells to repair similar damage to their mtDNA. The ability of karyotypically normal human fibroblasts (WI-38) and XP-A fibroblasts to repair alloxan-generated oxidative damage to nuclear and mtDNA was assessed using a quantitative Southern blot method in conjunction with the repair enzymes endonuclease III and formamidopyrimidine DNA glycosylase. The data indicate that both nuclear and mtDNA repair of each damage type investigated is more efficient in the WI-38 cells. These findings suggest a similarity between the process(es) used to repair oxidative damage to nuclear and mtDNA in that both are inhibited by the defect in XP-A.

¹ This work was supported in part by Grants ES 03456 and ES 0586 from the National Institute of Environmental Health Sciences and Grant AG 12442 from the National Institute of Aging.

² To whom requests for reprints should be addressed, at Department of Structural and Cellular Biology, University of South Alabama, Mobile, Alabama 36688.

Received 9/26/95. Accepted 1/12/96.

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