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The rising global burden of diseases linked to reactive oxygen and nitrogen species (ROS/RNS) - including inflammatory disorders, cancers, neurodegenerative conditions, and cardiovascular disease - has intensified interest in enzyme-mimicking nanomaterials (nanozymes) as tools to modulate cellular redox balance. Natural antioxidant enzymes, chiefly superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), are the principal enzymatic defenses against oxidative stress, but their clinical use is limited by poor stability, short half-life, and high cost. Nanozymes, producible at scale with tunable, stable activity, offer a promising alternative. This review is organized around a mechanistic distinction essential to the literature but frequently blurred: antioxidant nanozymes, which net-scavenge ROS through reversible redox cycling, versus pro-oxidant nanozymes, which net-generate ROS through Fenton-type chemistry. Cerium oxide nanoparticles (CeO₂ NPs) are examined as the prototypical antioxidant nanozyme, their SOD- and CAT-like activities arising from reversible Ce³⁺/Ce⁴⁺ cycling and oxygen-vacancy chemistry at the surface, with the Ce³⁺/Ce⁴⁺ ratio determining which activity predominates. Magnetite nanoparticles (Fe₃O₄ NPs) are examined as the prototypical pro-oxidant nanozyme, dominated by peroxidase-like Fenton chemistry driven by surface Fe²⁺/Fe³⁺ cycling that generates hydroxyl radicals, exploited for antibacterial and antitumour applications, with CAT-/SOD-like activity arising only as a secondary, concentration- and pH-dependent behaviour. Beyond mechanism, this review surveys the expanding application space for both classes, including ROS/analyte sensing, antibacterial therapy against resistant pathogens, diabetic wound healing, treatment of ROS-associated disease, and catalysis by related metal-oxide nanocatalysts. By keeping the two tracks mechanistically distinct, this review provides a clearer framework for rational nanozyme-based therapeutic design.