[en] The authors investigated the lethal, UV killing-potentiating and repair-inhibiting effects of trivalent arsenic trioxide (As₂O₃) and pentavalent sodium arsenate (Na₂HAsO₄) in normal human and xeroderma pigmentosum (XP) fibroblasts. The presence of As₂O₃ for 24 h after UV irradiation inhibited the thymine dimer excision from the DNA of normal and XP variant cells. Correspondingly, As₂O₃ also potentiated the lethal effect of UV on excision-proficient normal and XP variant cells in a concentration-dependent manner, but not on excision-defective XP group A cells. The above results provide the first evidence that arsenic inhibits the excision of pyrimidine dimers. Partially repair-suppressing small doses of As₂O₃ (0.5 μg/ml) and Na₂HAsO₄ (5 μg/ml) enhanced co-mutagenically the UV induction of 6-thioguanine-resistant mutations of V79 Chinese hamster cells. Thus, such a repair inhibition may be one of the basic mechanisms for the co-mutagenicity and presumably co-carcinogenicity of arsenic. (Auth.)