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体外吉田细胞系中对环磷酰胺和磷酰胺氮芥耐药的一种推测机制。

A proposed mechanism of resistance to cyclophosphamide and phosphoramide mustard in a Yoshida cell line in vitro.

作者信息

McGown A T, Fox B W

出版信息

Cancer Chemother Pharmacol. 1986;17(3):223-6. doi: 10.1007/BF00256688.

DOI:10.1007/BF00256688
PMID:3742706
Abstract

A Yoshida sarcoma cell line (YR/cyclo) showing decreased sensitivity to metabolically activated cyclophosphamide in vitro has been shown to be cross-resistant to phosphoramide mustard, the ultimate alkylating agent formed from cyclophosphamide. Resistance to these alkylating agents has been shown to be associated with increased activity of the glutathione S-transferase group of enzymes, and with elevated levels of glutathione, the cosubstrate of the enzyme. The resistant cell line shows lower levels of cellular damage, as measured by alkaline elution following treatment with phosphoramide mustard, than the parental (YS) line. The mechanism of resistance is ascribed to increased deactivation of potentially damaging metabolites of cyclophosphamide by the glutathione S-transferase enzymes, resulting in decreased cellular damage in the resistant cell line.

摘要

一种吉田肉瘤细胞系(YR/cyclo)在体外对代谢活化的环磷酰胺敏感性降低,已证明其对磷酰胺芥(由环磷酰胺形成的最终烷基化剂)具有交叉抗性。对这些烷基化剂的抗性已显示与谷胱甘肽S-转移酶组酶的活性增加以及该酶的共底物谷胱甘肽水平升高有关。与亲代(YS)细胞系相比,经磷酰胺芥处理后通过碱性洗脱测定,抗性细胞系显示出较低水平的细胞损伤。抗性机制归因于谷胱甘肽S-转移酶对抗环磷酰胺潜在损伤性代谢物的失活作用增强,从而导致抗性细胞系中细胞损伤减少。

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A proposed mechanism of resistance to cyclophosphamide and phosphoramide mustard in a Yoshida cell line in vitro.体外吉田细胞系中对环磷酰胺和磷酰胺氮芥耐药的一种推测机制。
Cancer Chemother Pharmacol. 1986;17(3):223-6. doi: 10.1007/BF00256688.
2
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Role of glutathione in cellular resistance to alkylating agents.谷胱甘肽在细胞对烷化剂的抗性中的作用。
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本文引用的文献

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Cancer Res. 1984 Nov;44(11):5156-60.
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