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Eukaryotic cells exposed to DNA damaging agents activate important defensive pathways by inducing multiple proteins involved in DNA repair, cell cycle checkpoint control and potentially apoptosis. After the acceptance of the hypothesis that oxidatively generated clustered DNA lesions (OCDL: closely spaced DNA lesions) can be induced even by low doses of ionizing radiation or even endogenously, and significant advances have been made in the understanding of the biochemistry underlying the repair of closely spaced DNA lesions, many questions still remain unanswered. The major questions that have to be answered in the near future are: 1) how human cells process these types of DNA damage if they repair them at all, 2) under what conditions a double strand break (DSB) may be created during the processing of two closely spaced DNA lesions and 3) what type of repair protein interactions govern the processing of complex DNA damage? The data existing so far on human cells and tissues are very limited and in some cases contradicting. All of them though agree however on the major importance of gaining mechanistic insights on the pathways used by the cell to confront and process complex DNA damage located in a small DNA volume and the need of more in depth analytical studies. We selectively review recently-obtained data on the processing of non-DSB DNA damage clusters in human cells and tissues and discuss the current status of knowledge in the field.
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