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Oxidative stress is defined as an imbalance between the production of oxygen reactive species (ROS) and their endogenous capacity of capturing them. Oxidative stress activates multiple effects generated by the non-specific growth of the ROS and by the decrease of antioxidant concentrations and neutralization mechanisms. The most accurate understanding of the mechanisms underlying oxidative stress and the deepening of its implications in different cancers has become very important in recent decades. Cancer cells are usually subjected to high levels of ROS, which continually activates the malignant phenotype by stimulating cell proliferation – by increasing the mitotic rate, angiogenesis, invasiveness and metastasis rates. The role of the ROS in the etiology and progression of breast cancer is in continuous processing. However, less attention has been paid to the development of redox-targeted breast cancer therapy strategies. Excess ROS production is detrimental for the survival and proliferation of neoplastic cells, through the oxidative-destructive mechanisms of biomolecules essential for life. This study departs from the hypothesis that the tumor is an inductive factor of oxidative stress, and an antioxidant treatment prior to surgery may influence the response to surgical treatment in breast cancer patients. This response is highlighted by determining certain essential compounds of the redox balance, after initiating the antioxidant therapy. Moreover, we have tried to assess the possible biochemical changes given by age, tumor size and asymmetry/laterality of the neoplasm in the investigated patients, and to determine the prognostic or predictive factors of these changes.

Production of Reactive Oxygen Species, Unbalanced by Endogenous Antioxidant Capture Mechanisms Monitored in Surgically Treated Breast Cancer