谷胱甘肽耗竭可逆转小鼠L1210白血病细胞对顺铂的耐药性。
Glutathione depletion reverses cisplatin resistance in murine L1210 leukemia cells.
作者信息
Hromas R A, Andrews P A, Murphy M P, Burns C P
出版信息
Cancer Lett. 1987 Jan;34(1):9-13. doi: 10.1016/0304-3835(87)90067-x.
PMID:3802072
Abstract
Little is understood about the mechanism of acquired resistance to the widely used antineoplastic drug, cisplatin. The cisplatin-resistant murine leukemia L1210 cell line L1210/PAM has an elevated cellular glutathione content, as compared to its sensitive parent cell line, L1210/. Exposure to D,L-buthionine-S,R-sulfoximine reduced L1210/PAM cells' glutathione content to nearly that of L1210/ cells and abrogated the resistance to cisplatin.
摘要
对于广泛使用的抗肿瘤药物顺铂的获得性耐药机制，人们了解甚少。与敏感的亲本细胞系L1210/*相比，顺铂耐药的小鼠白血病L1210细胞系L1210/PAM的细胞内谷胱甘肽含量升高。用D，L-丁硫氨酸-S，R-亚砜亚胺处理可使L1210/PAM细胞的谷胱甘肽含量降至接近L1210/*细胞的水平，并消除其对顺铂的耐药性。
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