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Colcemid, a drug initially for arresting cells at mitotic stage, was found to inhibit the rejoining of nucleotide excision repair (NER) in cells exposed to UV irradiation. Subsequent studies reveal not only colcemid but the chemicals which cause oxidative stress have the similar inhibitory effect on gap filling of NER. The inhibitory effect has been correlated to the base excision repair (BER) of oxidative DNA damage and was proposed to result from the competition between BER and NER for common components such as PCNA in the gap filling step. The proposition was supported by the observation that overexpression of PCNA attenuates the oxidative stress-induced inhibition of gap filling of NER. Considering the roles of PCNA in both repairing of oxidative DNA damage and translesion DNA synthesis, a model is proposed. Lastly, the chemistry of colcemid in causing oxidative stress is briefly reviewed.