Aphidicolin inhibits excision repair of UV-induced pyrimidine photodimers in low serum cultures of mitotic and mitomycin C-induced postmitotic human skin fibroblasts

Mutation Research/DNAging Pub Date : 1993-08-01 DOI:10.1016/0921-8734(93)90014-T

Hugo J. Niggli

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引用次数: 12

Abstract

The rates of formation and excision of UVC light-induced cyclobutane-type pyrimidine photodimers were determined in cultures of foreskin-derived normal human fibroblasts in mitotic (MF) and mitomycin-C (MMC)-induced postmitotic fibroblasts (PMF). Characteristic morphological changes support the notion that MMC accelerates the differentiation pathway from MF to PMF. In cultures treated with aphidicolin, I am able to show that this inhibitor of α and/or δ polymerases significantly inhibits the repair of pyrimidine photodimers in foreskin-derived mitotic and MMC-induced postmitotic fibroblasts in low serum cultures (0.5%) following UVC irradiation. Over the concentration range of 0–2 μg/ml of aphidicolin, there is a strong concentration-dependent inhibition of repair in cells treated with 10 J/m² of UVC and incubated with aphidicolin during the post-incubation time (0–24 h). The results demonstrate that pyrimidine photodimers are repaired in low serum cultures by an α- and/or δ-polymerase-dependent pathway. These data also imply that the fibroblast differentiation system is a very useful tool to unravel the complex mechanisms of UV-induced DNA damage and repair.

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在有丝分裂和丝裂霉素c诱导的有丝分裂后人皮肤成纤维细胞的低血清培养中，阿霉素抑制紫外线诱导的嘧啶光二聚体的切除修复

在有丝分裂(MF)和丝裂霉素c (MMC)诱导的有丝分裂后成纤维细胞(PMF)培养的包皮来源的正常人成纤维细胞中，测定了UVC光诱导的环丁烷型嘧啶光二聚体的形成和切除率。特征性形态学变化支持MMC加速从MF到PMF的分化途径的观点。在用aphidicolin处理的培养物中，我能够证明这种α和/或δ聚合酶抑制剂在UVC照射下显著抑制低血清培养(0.5%)包皮来源的有丝分裂和mmc诱导的有丝分裂后成纤维细胞中嘧啶光二聚体的修复。在0-2 μg/ml的浓度范围内，10 J/m2的UVC处理并与aphidicolin孵育后(0-24 h)，对细胞的修复有很强的浓度依赖性抑制作用。结果表明，在低血清培养中，嘧啶光二聚体通过α-和/或δ-聚合酶依赖途径修复。这些数据也暗示成纤维细胞分化系统是一个非常有用的工具来揭示紫外线诱导的DNA损伤和修复的复杂机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Mutation Research/DNAging

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