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首页> 外文期刊>Journal of Cancer Research and Clinical Oncology >Antioxidant enzymes are elevated in dimethylbenz(a)anthracene-induced neoplastic murine keratinocytes containing an active rasHa oncogene.
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Antioxidant enzymes are elevated in dimethylbenz(a)anthracene-induced neoplastic murine keratinocytes containing an active rasHa oncogene.

机译:在含有活性rasHa癌基因的二甲基苯并(a)蒽诱导的肿瘤鼠角质形成细胞中,抗​​氧化酶升高。

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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.
机译:在含有活性rasHa癌基因的原代小鼠角质形成细胞和肿瘤性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着提高。由肿瘤性角质形成细胞制备的细胞匀浆中的过氧化电位低于由正常角质形成细胞制备的细胞匀浆中的过氧化电位。一致地,发现赘生性308细胞系比正常角质形成细胞对由UV-B辐射诱导的细胞毒性更具抗性。本研究表明,增强的抗氧化剂防御系统可以保护启动细胞免受UV-B诱导的氧化应激的影响,并且增强的酶促抗氧化剂防御系统可能是促进肿瘤性角质形成细胞选择性生长的机制。

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