Glutathione(GSH)麩胱甘太是含Tripetide的半胱胺酸(Cysteine)，而OTZ是Cysteine的先驅物，其會增加GSH的合成；而BSO為γ-glutamyl cysteine合成的抑制劑，其會抑制GSH的合成；本試驗探討抗癌藥物平陽黴素作用後對KB細胞內GSH的影響、改變細胞內GSH的濃度後對平陽黴素細胞毒性的影響、細胞內GSH的濃度對平陽黴素引發KB細胞凋亡的影響。研究結果發現，平陽黴素會造成KB細胞內GSH值下降，GSH的消耗增加會促進細胞死亡且細胞死亡模式會由細胞壞死轉變為細胞凋亡。
The effects of intracellular glutathione (GSH) concentration on the toxicity of pingyangmycin in human squamous cell carcinoma cell line were evaluated. By using the GSH synthesis inhibitor D,L-buthionine-S,R-sulfoximine (BSO) and the precursor of cysteine 2-oxothiazolidine-4-carboxylate (OTZ), intracellular glutathione levels were artificially changed. After exposed to different GSH concentrations cultured tumor cells were treated with pingyangmycin and the resultant mode of cell death was analyzed using morphological and biochemical criteria. It was found that the toxicity of pingyangmycin was obviously increased to cultured tumor cells on lowering GSH levels, with the mode of cell death switching from necrosis to apoptosis. In contract, treatment with OTZ increased GSH level compared with that of control cells, inhibited cell death induced by pingyangmycin via a necrotic rather than apoptotic process. These observations suggest that modulation of GSH levels effects the toxicity of pingyangmycin and that GSH influences the mode of cell death induced by pingyangmycin.
