代谢改变被认为是癌症的标志之一。其中，线粒体功能的改变与活性氧 (ROS) 产生的增强有关，活性氧会激活 ROS 调节的癌细胞信号通路。乳腺癌是全球女性癌症相关死亡的主要原因。它是一种异质性疾病，其亚型具有特定的分子特征和患者结果。为了确定非致瘤性、雌激素受体阳性 (ER) 和三阴性 (TN) 乳腺癌细胞能量代谢和氧化应激管理系统的差异，我们评估了 ROS 产生、蛋白酶水平和活性，并分析了能量代谢。我们发现非致瘤细胞和癌细胞之间以及 ER 和 TN 乳腺癌细胞之间的能量代谢和 ROS 管理系统存在差异。我们的结果表明，尽管所有测试的癌细胞系中糖酵解 ATP 水平不同，但仍依赖于糖酵解。此外，我们的数据表明，TN 细胞中高水平的 ROS 是由于 NADPH 生成系统和 GSH 系统的抗氧化能力有限、线粒体功能障碍和非线粒体 ROS 生成导致的，这使得 TN 细胞对 GSH 合成抑制剂更加敏感。我们的数据表明，乳腺癌的代谢和抗氧化分析将为乳腺癌治疗的代谢抑制剂或抗氧化治疗提供重要靶点。

Metabolic alterations are recognized as one of the hallmarks of cancer. Among these, alterations in mitochondrial function have been associated with an enhanced production of Reactive Oxygen Species (ROS), which activate ROS-regulated cancer cell signaling pathways. Breast cancer is the main cancer-related cause of death for women globally. It is a heterogeneous disease with subtypes characterized by specific molecular features and patient outcomes. With the purpose of identifying differences in energy metabolism and the oxidative stress management system in non-tumorigenic, estrogen receptor positive (ER+) and triple negative (TN) breast cancer cells, we evaluated ROS production, protein enzyme levels and activities and profiled energy metabolism. We found differences in energetic metabolism and ROS management systems between non-tumorigenic and cancer cells and between ER+ and TN breast cancer cells. Our results indicate a dependence on glycolysis despite different glycolytic ATP levels in all cancer cell lines tested. In addition, our data show that high levels of ROS in TN cells are a result of limited antioxidant capacity in the NADPH producing and GSH systems, mitochondrial dysfunction and non-mitochondrial ROS production, making them more sensitive to GSH synthesis inhibitors. Our data suggest that metabolic and antioxidant profiling of breast cancer will provide important targets for metabolic inhibitors or antioxidant treatments for breast cancer therapy.