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在含有活性rasHa癌基因的二甲基苯并[a]蒽诱导的肿瘤性小鼠角质形成细胞中,抗氧化酶水平升高。

Antioxidant enzymes are elevated in dimethylbenz[a]anthracene-induced neoplastic murine keratinocytes containing an active rasHa oncogene.

作者信息

Lehtola K, Laurikainen L, Leino L, Ahotupa M, Punnonen K

机构信息

Department of Clinical Chemistry, University Central Hospital of Turku, Finland.

出版信息

J Cancer Res Clin Oncol. 1995;121(7):402-6. doi: 10.1007/BF01212946.

Abstract

Antioxidant enzyme activities and peroxidation potential were measured in primary mouse keratinocytes and neoplastic keratinocytes containing an active rasHa oncogene. In neoplastic cell lines, SP-1 and 308, the activities of Cu, Zn-superoxide dismutase, catalase, and glutathione transferase were significantly elevated. The peroxidation potential was lower in cell homogenates prepared from neoplastic keratinocytes than in those prepared from normal keratinocytes. Consistently, the neoplastic 308 cell line was found to be more resistant than the normal keratinocytes to cytotoxicity induced by UV-B irradiation. The present study suggests that the enhanced antioxidant defense system protects the initiated cells from UV-B-induced oxidative stress, and that the enhanced enzymic antioxidant defense system is potentially a mechanism favoring the selective growth of neoplastic keratinocytes.

摘要

在原代小鼠角质形成细胞和含有活性rasHa癌基因的肿瘤角质形成细胞中测量了抗氧化酶活性和过氧化潜力。在肿瘤细胞系SP-1和308中,铜锌超氧化物歧化酶、过氧化氢酶和谷胱甘肽转移酶的活性显著升高。肿瘤角质形成细胞制备的细胞匀浆中的过氧化潜力低于正常角质形成细胞制备的细胞匀浆。一致地,发现肿瘤308细胞系比正常角质形成细胞对UV-B辐射诱导的细胞毒性更具抗性。本研究表明,增强的抗氧化防御系统可保护起始细胞免受UV-B诱导的氧化应激,并且增强的酶促抗氧化防御系统可能是一种有利于肿瘤角质形成细胞选择性生长的机制。

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