## 1 Introduction
cellular redox balance and protein homeostasis, leading to a significant increase in GSH level, reduction in GSSG/GSH ratio, and a decrease in reduced free thiol content [20]. Although free radicals are generally present inside our body, damages to cellular components, e.g., lipids, proteins, and DNA, occur when the balance between produced and scavenged radical species is impaired [21]. Several endogenous molecules, such as antioxidant enzymes (glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), thioredoxin reductase (TRx), and peroxideroxin (PRx)), together with food-borne exogenous antioxidant molecules (such as resveratrol and other polyphenols) help to maintain the redox homeostasis. When this homeostasis is disrupted and free radicals are in excess, they can cause lipid peroxidation, damages to cellular membranes and lipoproteins, alterations to proteins, and DNA mutations. The most representative one involves the formation of 8-hydroxyguanosine (8-OHG), which is oxidized to 8-hydroxy-2\({}^{\prime}\)-deoxyguanosine (8-OHdG) [22]. Similarly, 4-hydroxymonenal (4-HNE) and malonaldehyde (MDA), derived from lipid peroxidation, react with DNA, yielding etheno-DNA base adducts that compromise the correct replication process. Uncontrolled oxidative stress can induce or help to develop several pathologies, such as cardiovascular, neurodegenerative, and respiratory diseases [23; 24; 25]. Free radicals can interact with several signaling pathways, for example, the mitogen-activated protein kinase (MAPK), signaling pathways regulating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) factor, phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR (mechanistic target of rapamycin), and other transcription factors, such as the signal transducer and activator of transcription 3 (STAT3), hypoxia-inducible factor 1-alpha (HIF-1\(\alpha\)), and p53 [26; 27; 28; 29]. Furthermore, NF-kB and the nuclear factor erythroid 2-related factor 2 (Nrf2), which modulates the gene expression of numerous antioxidant enzymes, interplay through a range of complex molecular interactions, thus participating to balance the cellular redox status and the response to stress and inflammation [30]. Numerous studies have also demonstrated the involvement of ROS in the epithelial-mesenchymal transition (EMT), characterized by the activation of mesenchymal markers, such as metalloproteinases and transforming growth factor-\(\beta\) (TGF-\(\beta\)), and by a simultaneous decrease in the expression levels of epithelial markers, such as E-cadherin and \(\gamma\)-catenin [31; 32]. Finally, it has been shown that high levels of ROS modulate the angiogenesis process by interacting with numerous signal cascades, which lead to the activation of transcription factors, such as vascular endothelial growth factor (VEGF) and HIF-1\(\alpha\)[33; 34]. VEGF is produced by cells to stimulate the growth of new blood vessels and can induce angiogenesis by stimulating the proliferation and migration of endothelial cells. Although high levels of ROS are implicated in oxidative DNA damage and subsequent carcinogenesis, these reactive species can also act as anti-tumorigenic agents by promoting cell death, permeabilizing the mitochondrial membrane, and inducing the release of cytochrome c into the cytosol, where it forms complexes called apoptosomes, with cytosolic proteins, such as Apaf-1. These complexes activate caspase-9, which in turn triggers effector caspases, such as caspase-3, thus initiating the apoptotic process [35; 36]. Breast cancer is the most common cancer type in women (30% of female cancers in 2020), with increasing global incidence and number of deaths [37]. Several genetic and non-genetic factors, such as obesity and excessive alcohol consumption, can contribute to the development of this pathology [38].