<p>Intermittent fasting (IF) has gained increasing attention as a lifestyle intervention potentially influencing metabolic health and aging, partly through modulation of oxidative stress. This narrative review synthesizes current evidence on the effects of IF on oxidative pathways at molecular, cellular, and clinical levels. Mechanistically, IF induces metabolic switching from glucose to fatty acid and ketone utilization, activating interconnected nutrient-sensing pathways such as AMPK, SIRT1, and NRF2, as well as autophagy, which collectively contribute to improved mitochondrial function, enhanced antioxidant defenses, and reduced reactive oxygen species production. Preclinical studies consistently demonstrate that IF can reduce oxidative damage, upregulate endogenous antioxidant systems, and improve cellular stress resilience. However, much of this mechanistic evidence is derived from animal and experimental models, and its direct translation to humans remains uncertain. Human studies, including Ramadan cohorts and small interventional trials, report modest changes in commonly used oxidative stress biomarkers such as malondialdehyde (MDA) and F₂-isoprostanes. Nevertheless, these markers are non-specific, subject to methodological variability, and do not fully reflect tissue-level redox dynamics or clinically meaningful outcomes. Overall, human evidence remains limited, heterogeneous, and largely based on short-term studies, with a lack of long-term randomized controlled trials evaluating clinically relevant endpoints. While IF shows biologically plausible effects on oxidative stress, its clinical significance remains uncertain. Further well-designed, long-duration trials with standardized and comprehensive redox assessments are required to clarify its translational relevance.</p>