stages (IIIB-IV), a multidisciplinary treatment is the most common practice. Platinum-based chemotherapy alone or combined with radiotherapy has been used in most treatment protocols [8], cisplatin being one of the most common platinum analogs used. The mode of action of cisplatin consists of binding to nuclear DNA thereby creating DNA adducts. Particularly, cisplatin reacts with the N-7 of purines, generating intra- and inter-strand cross-links [9] and, consequently, blocks replication and transcription, which results in cell death by necrosis or apoptosis [10]. However, this mode of action leads to an indiscriminate attack on all rapidly dividing cells, which results in well-established adverse side effects. The most common side effects include nephrotoxicity, ototoxicity, neurotoxicity, and vomiting [10; 11; 12]. Moreover, the development of resistance of cancer cells to cisplatin and its analogs is a major issue [12]. Oxidative stress is present in several pathologies, including cancer [13], and there have been several reports addressing this topic. Higher concentrations of reactive oxygen species (ROS) are commonly found in cancer cells when compared with normal cells [14; 15; 16]. More specifically, these cells have a generally lower capability to remove hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) [17]. The ability to detoxify H\({}_{2}\)O\({}_{2}\) depends largely on the levels of catalase (CAT), glutathione peroxidase (GPx), and peroxideroxins (PRDX) [18]. These enzymes are either present at lower levels in malignant cells or are inactivated. Such a situation enables cancer cells to employ ROS for their own benefit, i.e., survival and proliferation. Yet, the balance is delicate, and if the ROS are pushed to very high levels, they would become cytotoxic to cancer cells and would force them to undergo apoptosis/ necrosis [19]. Thus, different approaches to redox modulation that further increase the concentrations of ROS, particularly H\({}_{2}\)O\({}_{2}\), are advantageous in a therapeutic context. This concept has been termed redox-directed cancer therapy [20] and is a promising strategy to enhance the efficacy of chemotherapy in suppressing the growth of these cells. Using native superoxide dismutases (SOD) was formerly suggested as a possible therapeutic strategy [21; 22]. These enzymes are responsible for the dismutation of superoxide anion (O\({}_{2}\)\({}^{\bullet-}\)), thus accumulating H\({}_{2}\)O\({}_{2}\). The clinical use of native SOD has its disadvantages, such as elevated manufacturing costs, low permeability, high immunogenicity, and short half-life [23]. To overcome these disadvantages, SOD mimics (SODm) were initially created. These are synthetic compounds with the ability to mimic the properties of native SOD enzymes [24]. SODm are capable of disproportionating O\({}_{2}\)\({}^{\bullet-}\) and also possess scavenging properties towards other reactive species, such as ONOO\({}^{-}\) and NO\({}_{2}\)[14]. These compounds may also increase the amount of H\({}_{2}\)O\({}_{2}\) present in the cells either via O\({}_{2}\)\({}^{\bullet-}\) dismutation or cycling with cellular reductants [25], and most so in cancer cells where the H\({}_{2}\)O\({}_{2}\)-removing systems are deficient. This could push H\({}_{2}\)O\({}_{2}\) concentration to the toxicity limit, reducing proliferation and increasing the efficiency of chemotherapy and radiotherapy [14; 26; 27]. Apart from these benefits, SODm can also protect healthy cells against the adverse effects of chemo/radiotherapy since, in general, as abovementioned, non-malignant cells display higher basal levels of antioxidants, therefore counteracting the increase in H\({}_{2}\)O\({}_{2}\) levels. In this sense, the SODm have a dual role [14; 23], being currently considered modulators of cellular transcriptional activity in both cancer and healthy cells [28]. Manganese porphyrins (MnPs) are one of the most promising classes of SODm. These porphyrins are highly stable and can penetrate cellular membranes due to their low molecular weight [28].