Groen H J, Meijer C, De Vries E G, Mulder N H
Department of Pulmonary Diseases, University Hospital, Groningen, The Netherlands.
Anticancer Res. 1996 Mar-Apr;16(2):1033-7.
Intrinsic resistance in non-small cell lung cancer (NSCLC) curtails the efficacy of chemotherapy and radiotherapy. Glutathione (GSH) may be one of the factors responsible for this phenomenon as it counteracts the cytotoxic effects of platinum containing drugs and radiation. GSH levels were studied in red blood cells of seven smoking patients with NSCLC treated with continuously infused carboplatin and concomitant radiotherapy for 6 weeks. The levels of red blood cell GSH remained unchanged during prolonged combined treatment and were similar to those in non-smoking volunteers. In vitro, in a cell-free system, it was demonstrated that GSH-platinum complex formation occurred with both cisplatin and carboplatin in a time-dependent manner and that this formation decreased total GSH as measured with Tietze's method. This implies that increased consumption of GSH by platinum and free radicals produced by carboplatin and radiation, respectively, seems to induce GSH in red blood cells resulting in an unchanged total GSH level. Although GSH in red blood cells may be relevant as a detoxification pool for platinum, it had no impact on response rates in these patients with NSCLC.
非小细胞肺癌（NSCLC）的内在抗性会降低化疗和放疗的疗效。谷胱甘肽（GSH）可能是导致这种现象的因素之一，因为它能抵消含铂药物和辐射的细胞毒性作用。对7名吸烟的NSCLC患者的红细胞谷胱甘肽水平进行了研究，这些患者接受持续输注卡铂并同时进行放疗，为期6周。在长期联合治疗期间，红细胞谷胱甘肽水平保持不变，且与非吸烟志愿者的水平相似。在体外无细胞系统中，已证明顺铂和卡铂均能以时间依赖性方式形成谷胱甘肽 - 铂复合物，并且这种形成会降低用蒂茨方法测得的总谷胱甘肽水平。这意味着，分别由卡铂和辐射产生的铂和自由基对谷胱甘肽的消耗增加，似乎会诱导红细胞中的谷胱甘肽，从而使总谷胱甘肽水平保持不变。尽管红细胞中的谷胱甘肽可能作为铂的解毒池具有相关性，但它对这些NSCLC患者的反应率没有影响。
