Filippova V G, Chekova V V, L'vova G N, Vasil'eva I M, Sinel'shchikova T A, Gubitskaia E G, Balkarov I M, Zasukhina G D
Ter Arkh. 1990;62(6):79-81.
DNA repair was explored in continuous cells withdrawn from gout patients. The data obtained were compared to those on primary cells (lymphocytes) from the same patients. Two continuous lines of fibroblasts obtained from the biopsy material of patients suffering from gout were examined for stability of reparation defects on long cell passage. The studies were made with 4 to 12 passages of patients' fibroblasts. The use of criteria reflecting certain stages of DNA repair (reparative synthesis of DNA, formation of induced DNA ruptures and their resynthesis during cell postincubation, reactivation and induced mutagenesis of measles vaccine virus in patients' cells) allowed confirmation of repair defect stability in gout patients' cells on their long passage. Based on the data on preservation of the repair defect on cell passage it is concluded that gout patients demonstrate the genetically determined impairment of the synthesis of DNA repair enzymes participating in the recovery of DNA impairments induced by UV radiation or UV mimetics.
对从痛风患者体内提取的连续传代细胞的DNA修复情况进行了研究。将获得的数据与同一患者原代细胞（淋巴细胞）的数据进行了比较。对从痛风患者活检材料中获得的两株成纤维细胞连续系进行了长期传代时修复缺陷稳定性的检测。对患者成纤维细胞传代4至12次进行了研究。通过反映DNA修复某些阶段的标准（DNA的修复合成、诱导性DNA断裂的形成及其在细胞孵育后重新合成、麻疹疫苗病毒在患者细胞中的再激活和诱导诱变），证实了痛风患者细胞在长期传代时修复缺陷的稳定性。基于细胞传代时修复缺陷保留的数据得出结论，痛风患者表现出参与紫外线辐射或紫外线模拟物诱导的DNA损伤修复的DNA修复酶合成的遗传决定损伤。
