Asian Journal of Current Research

The transition from late gestation to established lactation imposes an abrupt and severe metabolic reorganisation on the dairy cow, and redox imbalance has become one of the dominant explanatory frameworks for the clustering of metabolic and infectious disease that accompanies it. Three decades of research have established that periparturient cows experience increased production of reactive oxygen and nitrogen species alongside variable depletion of antioxidant defences, yet the field has advanced unevenly. Mechanistic work has progressed rapidly towards organelle-level processes including mitochondrial dysfunction, impaired mitophagy, regulated iron-dependent cell death and transcriptional control through the nuclear factor erythroid 2-related factor 2 pathway, whereas herd-level intervention studies continue to rely on assays of uncertain specificity and to report inconsistent, occasionally opposing, outcomes. This critical narrative review evaluates the strength, coherence and limitations of the evidence linking oxidative stress to transition cow health, and examines why mechanistic plausibility has not translated reliably into demonstrated efficacy of antioxidant supplementation. Literature was identified through structured searching of general and scholarly web resources together with bibliographic verification, and appraised for design adequacy, measurement validity and analytical transparency rather than aggregated quantitatively. The evidence most securely supports the conclusions that oxidant exposure rises around parturition, that lipid mobilisation and hepatic fatty acid oxidation are principal drivers, and that antioxidant supplementation benefits animals whose antioxidant status is genuinely inadequate. Evidence is considerably weaker for the propositions that a single circulating biomarker adequately represents tissue redox state, that supplementation improves outcomes in already-replete herds, and that redox imbalance is causally upstream rather than concurrent with metabolic and inflammatory dysregulation. Analytical heterogeneity, small experimental units, reliance on healthy cohorts and scarce reporting of baseline antioxidant status emerge as the principal obstacles to synthesis. Priorities include harmonised biomarker panels anchored on lipid peroxidation products of established specificity, adequately powered trials stratified by pre-treatment antioxidant status, and tissue-level validation of mechanisms currently characterised mainly in vitro.