# Biosynthesis of Zinc Oxide Nanoparticles Using Seaweed: Exploring Their Therapeutic Potentials
## 4 Discussion
The amount of TAC measured was impacted by the molybdenum reduction [51]. The ability of ZnO-NPs to change from ferric (III) to ferrous (II) in a redox-linked colorimetric process involving a single electron transfer has been used to measure the antioxidant activity of these particles using FRAP [52]. In order to suppress reactive species, antioxidants biologically transfer an electron or hydrogen (H) atom to them [53]. Thus, the antioxidant potential can be evaluated using hydrogen atom transfer (HAT) and single-electron transfer-dependent assays (SET). SET assays are used to measure an antioxidant's capacity to lessen an oxidant, which undergoes a color change when reduced. SET assays such as total antioxidant capacity (TAC) and ferric reducing antioxidant power (FRAP) tests could be used to quantify the reduced capacity. Nevertheless, the phosphor-molybdenum and FRAP experiments showed that the NPs had strong, considerable antioxidant potential. It should be emphasized that in the phosphor-molybdenum and ferrozine experiments, electron transfer occurs at different redox potentials, and in both cases, the structure of the antioxidant (ZnO-NPs) being studied controls the reducing activity. To figure out whether the studied nanoparticles could be used safely for treatment, cytotoxicity studies of the ZnO-NPs were performed. Based on the decreased viability of the investigated cell lines following incubation with the nanoparticles at increasing concentrations, the cytotoxicity of the ZnO-NPs was calculated. First, the cytotoxicity was assayed using the MTT test. This investigation showed that the vitality of the treated cell lines was dose-dependent; it reduced with increasing NP concentrations. This result was consistent with those of earlier investigations [54]. The outcomes showed that at larger concentrations of the nanoparticles, i.e., 25, 50, and 100 g/mL, the viability of the cells considerably decreased. These outcomes were comparable to those obtained in ref. [55]. The biosynthesized ZnO-NPs of _U. lactuca_ were more effective on the MCF-7 cell line than on the HepG-2 and HCT-116 cell lines, recording a cell viability percentage of 24.6%. Higher ZnO-NP concentrations had a stronger inhibitory impact, almost completely killing the cells. This showed that the release of zinc ions (Zn+) from the particle surface and their subsequent adsorption to the surfaces of the cells as a source of toxic Zn+ ions, or the formation of toxic Zn+ ions through oxidative dissolution in the presence of oxygen, ligands, or organisms, is the main mechanism of ZnO-NP cytotoxicity on MCF-7 [47]. The new biomaterial is safe to use as an alternative material for a new anti-tumor and anti-microbial medicine, according to ZnO-NPs' cytotoxic impact [56]. A multi-step process, carcinogenesis involves both mutation and enhanced cell proliferation [57]. ROS overproduction compromises antioxidant defenses, and defective DNA repair processes can result in oxidative damage to cellular macromolecules [57]. ROS easily oxidize cellular fatty acids to create lipid peroxyl radicals and lipid hydroperoxides, which grow into MDA. Their suggested antioxidant activity is one of the potential methods through which ZnO-NPs exert their anti-tumor actions. This is supported by the results of the current study, which revealed that after the administration of ZnO-NPs, TAC greatly increased and MDA dramatically decreased compared to the control group [58]. Although the Dox treatment efficiently reduced tumor burden, it also resulted in much higher TAC and lower MDA levels when compared to the normal control group. This was consistent with the research in ref. [59], which showed that Dox generated oxidative stress throughout the body. Apoptosis induction in various tumors is another potential method through which ZnO-NPs exercise their anti-tumor effects [60]. Apoptosis is a method through which cells die in a controlled manner. A characteristic of cancer is apoptosis resistance.