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https://www.selleckchem.com/products/endoxifen-hcl.html Strictly regulated balance between the formation and utilization of reactive oxygen species (ROS) is the basis of normal functioning of organisms. ROS play an important role in the regulation of many metabolic processes; however, excessive content of ROS leads to the development of various disorders, including oncological diseases, as a result of ROS-induced mutations in DNA. In tumors, high levels of oxygen radicals promote cell proliferation and metastasis. On the other hand, high content of ROS can trigger cell death, a phenomenon used in the antitumor therapy. Water- and lipid-soluble antioxidants, as well as antioxidant enzyme systems, can inhibit ROS generation; however, they should be used with caution. Antioxidants can suppress ROS-dependent cell proliferation and metastasis, but at the same time, they may inhibit the death of tumor cells if the antitumor therapeutic agents stimulate oxidative stress. The data on the role of antioxidants in the death of tumor cells and on the effects of antioxidants taken as dietary supplements during antitumor therapy, are contradictory. This review focuses on the mechanisms by which antioxidants can affect tumor and healthy cells.BNIP3 is a member of Bcl-2 protein family involved in regulation of various forms of cell death. However, its role in these processes remains unclear and varies depending on the type of cancer cells and environmental factors (pH, O2 level, etc.). Here, the role of BNIP3 in apoptosis regulation in lung adenocarcinoma cells was investigated. The suppressed expression of BNIP3 caused inhibition of oxygen consumption and stimulated production of the mitochondrial reactive oxygen species, suggesting the role of BNIP3 in induction of mitochondrial dysfunction and its potential involvement in regulation of cell death. Indeed, cytochrome c release in the cells with BNIP3 knockout and knockdown was higher than in the wild-type (WT) upon apoptosis stim

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