2I. M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia
3Division of Toxicology, Institute of Environmental Medicine, Karolinska Institute, 171 77 Stockholm, Sweden
* To whom correspondence should be addressed.
Received July 14, 2020; Revised August 7, 2020; Accepted August 7, 2020
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.
KEY WORDS: cancer, antioxidants, carcinogenesis, reactive oxygen species, programmed cell death, mitochondria