Reactive Oxygen Species and Antioxidants in Carcinogenesis and Tumor Therapy
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REVIEW
Reactive Oxygen Species and Antioxidants in Carcinogenesis and Tumor Therapy S. M. Vostrikova1,2, A. B. Grinev2, and V. G. Gogvadze1,3,a* 1
Faculty of Medicine, Lomonosov Moscow State University, 119192 Moscow, Russia 2 I. M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia 3 Division of Toxicology, Institute of Environmental Medicine, Karolinska Institute, 171 77 Stockholm, Sweden a email: [email protected] Received July 14, 2020 Revised August 7, 2020 Accepted August 7, 2020 Abstract—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 lipidsoluble antioxidants, as well as antioxidant enzyme systems, can inhibit ROS generation; however, they should be used with cau tion. Antioxidants can suppress ROSdependent 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 contra dictory. This review focuses on the mechanisms by which antioxidants can affect tumor and healthy cells. DOI: 10.1134/S0006297920100132 Keywords: cancer, antioxidants, carcinogenesis, reactive oxygen species, programmed cell death, mitochondria
INTRODUCTION Tumor development is a multistage process character ized by certain disorders of cellular metabolism. Hanahan and Weinberg [1] identified 10 physiological hallmarks that distinguish tumor and normal cells. One of them is sup pression of programmed cell death (PCD), which normal ly allows tissues to eliminate obsolete cells (cells that have fulfilled their functions), as well as defective and potential ly dangerous cells. Dysregulation of this process might cause tumor development. One of the most studied forms of PCD is apoptosis, which prevents accumulation of cells with genetic abnormalities, thereby averting their malig nant transformation. Stimulation of apoptosis in tumor cells is an effective anticancer therapy strategy. Other than Abbreviations: GPx, glutathione peroxidase; HIF, hypoxia inducible factor; MAO, monoamine oxidase; MPT, mitochon drial permeability transition; ROS, reactive oxygen species; NFκB, nuclear factor κB; NOX, NADPH oxidase; PCD, pro grammed cell death; SOD, superoxide dismutase; TNF, tumor necrosis factor. * To whom correspondence should be addressed.
apoptosis
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