Delpino A, Nista A, Marcante M L, Ferrini U, Silvestrini B, Caputo A, Floridi A
Exp Mol Pathol. 1986 Apr;44(2):197-206. doi: 10.1016/0014-4800(86)90070-5.
The ability of lonidamine [1-(2,4)-dichlorobenzyl-1H-indazol-3-carboxylic acid], to induce a stress response in human and murine cultured melanoma cells has been demonstrated. In the M14 and M10 human melanoma cell lines, lonidamine enhances the synthesis of a unique set of proteins, characterized by SDS-PAGE by an Mr of about 72 kDa. In the B16 murine melanoma cell line, exposure to lonidamine increases the synthetic rate of two polypeptides of mol mass 86 and 72 kDa, respectively. Lonidamine is a drug which specifically acts on mitochondria. Therefore the observation that it can also promote a stress response indicates that the mitochondria might be one of the primary cellular targets and postulates a causal relationship between an impairment of the energy supply and induction of stress protein synthesis.
已证实氯尼达明[1-(2,4)-二氯苄基-1H-吲唑-3-羧酸]能够在人源和鼠源培养的黑色素瘤细胞中诱导应激反应。在M14和M10人黑色素瘤细胞系中，氯尼达明可增强一组独特蛋白质的合成，通过SDS-PAGE分析其分子量约为72 kDa。在B16鼠黑色素瘤细胞系中，暴露于氯尼达明会分别增加分子量为86 kDa和72 kDa的两种多肽的合成速率。氯尼达明是一种特异性作用于线粒体的药物。因此，它还能促进应激反应这一观察结果表明，线粒体可能是主要的细胞靶点之一，并假定能量供应受损与应激蛋白合成诱导之间存在因果关系。
