Cancer cells produce high levels of mitochondria-associated reactive oxygen species (ROS) that can damage macromolecules, but also promote cell signaling and proliferation. Therefore, mitochondria-targeted antioxidants have been suggested to be useful in anti-cancer therapy, but no studies have convincingly addressed this question. Here, we administered the mitochondria-targeted antioxidants MitoQ and MitoTEMPO to mice with BRAF-induced malignant melanoma and KRAS-induced lung cancer, and found that these compounds had no impact on the number of primary tumors and metastases; and did not influence mitochondrial and nuclear DNA damage levels. Moreover, MitoQ and MitoTEMPO did not influence proliferation of human melanoma and lung cancer cell lines. MitoQ and its control substance dTPP, but not MitoTEMPO, increased glycolytic rates and reduced respiration in melanoma cells; whereas only dTPP produced this effect in lung cancer cells. Our results do not support the use of mitochondria-targeted antioxidants for anti-cancer monotherapy, at least not in malignant melanoma and lung cancer.

中文翻译：

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线粒体靶向抗氧化剂MitoQ和MitoTEMPO不会影响BRAF驱动的恶性黑色素瘤和KRAS驱动的肺癌的进展。

癌细胞产生高水平的线粒体相关活性氧（ROS），可破坏大分子，但也会促进细胞信号传导和增殖。因此，线粒体靶向抗氧化剂已被认为可用于抗癌治疗，但尚无研究令人信服地解决该问题。在这里，我们将线粒体靶向抗氧化剂MitoQ和MitoTEMPO应用于患有BRAF诱导的恶性黑色素瘤和KRAS诱导的肺癌的小鼠，发现这些化合物对原发肿瘤和转移的数量没有影响。并且不影响线粒体和核DNA损伤水平。此外，MitoQ和MitoTEMPO不会影响人黑素瘤和肺癌细胞系的增殖。MitoQ及其控制物质dTPP，但不是MitoTEMPO，黑色素瘤细胞中糖酵解速率增加，呼吸减少；而只有dTPP在肺癌细胞中产生这种作用。我们的结果不支持将针对线粒体的抗氧化剂用于抗癌单一疗法，至少在恶性黑色素瘤和肺癌中不适用。