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8-甲氧基补骨脂素加紫外线A辐射诱导C3H小鼠胚胎10T1/2细胞发生肿瘤转化

Neoplastic transformation of C3H mouse embryo 10T1/2 cells by 8-methoxypsoralen plus UVA radiation.

作者信息

Ananthaswamy H N

出版信息

J Invest Dermatol. 1985 Aug;85(2):102-6. doi: 10.1111/1523-1747.ep12276467.

DOI:10.1111/1523-1747.ep12276467
PMID:4020157
Abstract

The effect of 8-methoxypsoralen plus UVA radiation (PUVA) on cell killing and induction of transformation was studied in the C3H mouse embryo 10T1/2 cell line. Dose-response data for both survival and transformation were obtained as a function of 8-methoxypsoralen (8-MOP) concentration and UVA dose. PUVA treatment caused cell death and induced transformation in a dose-dependent manner. Treatment of cells with 8-MOP alone (10 micrograms/ml) or UVA alone (90 J/m2) had no effect on either cell killing or transformation. The product of 8-MOP concentration and UVA dose calculated at 10% survival and 10(-3) transformation frequency levels were quite similar regardless of 8-MOP concentration or UVA dose. This suggests that there exists a simple reciprocal relationship between 8-MOP concentration and UVA dose. Both type II and type III foci induced by PUVA treatment were tumorigenic in vivo. These data provide further evidence for the carcinogenicity of PUVA treatment. In addition, the system described here could serve as a valuable model for studying the relationships between transformation and the specific cellular and molecular lesions induced by PUVA treatment.

摘要

在C3H小鼠胚胎10T1/2细胞系中研究了8-甲氧基补骨脂素加紫外线A辐射(PUVA)对细胞杀伤和转化诱导的影响。获得了存活和转化的剂量反应数据,作为8-甲氧基补骨脂素(8-MOP)浓度和紫外线A剂量的函数。PUVA处理以剂量依赖性方式导致细胞死亡并诱导转化。单独用8-MOP(10微克/毫升)或单独用紫外线A(90焦/平方米)处理细胞对细胞杀伤或转化均无影响。无论8-MOP浓度或紫外线A剂量如何,在10%存活和10^(-3)转化频率水平下计算的8-MOP浓度与紫外线A剂量的乘积相当相似。这表明8-MOP浓度与紫外线A剂量之间存在简单的反比关系。PUVA处理诱导的II型和III型病灶在体内均具有致瘤性。这些数据为PUVA处理的致癌性提供了进一步的证据。此外,这里描述的系统可作为研究转化与PUVA处理诱导的特定细胞和分子损伤之间关系的有价值模型。

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引用本文的文献

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Signature p53 mutation at DNA cross-linking sites in 8-methoxypsoralen and ultraviolet A (PUVA)-induced murine skin cancers.8-甲氧基补骨脂素和紫外线A(PUVA)诱导的小鼠皮肤癌中DNA交联位点的特征性p53突变
Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7961-5. doi: 10.1073/pnas.93.15.7961.