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Abstract Oxidative stress plays a key role in bipolar disorder (BD). 8,5’-cyclopurine-2’-deoxynucleosides (cPUs), including R- and S-cdA, are tandem oxidative lesions that distort the DNA helix, impair replication and transcription, and are primarily repaired by the nucleotide excision repair (NER) pathway. To date, cPU levels and NER gene expressions have not yet been studied in BD.
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