Terminalia buceras (Syn. Bucida buceras) and Retinal Oxidative Stress: A Critical Review of Published Evidence and Its Relevance to Dry Age-Related Macular Degeneration

Abstract

Dry age-related macular degeneration (dAMD) is a multifactorial retinal disorder involving oxidative stress, mitochondrial dysfunction, chronic para-inflammation, complement dysregulation, and progressive retinal pigment epithelium (RPE) failure. This critical review evaluates the published evidence concerning Terminalia buceras (L.) C.Wright (syn. Bucida buceras L.; Combretaceae), hereafter referred to as T. buceras, and its relevance to dry age-related macular degeneration. The evidence is organized into five categories: species-specific chemical evidence, species-specific retinal evidence, species-specific non-retinal biological evidence, external isolated-compound evidence, and hypothesis-generating comparisons with related plants or experimental systems. The evidence base remains preliminary. Species-specific retinal data are restricted to in vitro observations, and there are currently no epidemiological studies linking T. buceras use to AMD outcomes, no validated animal studies demonstrating efficacy in dAMD, and no clinical studies. Moreover, phytochemical standardization, ocular exposure, metabolism, and retinal bioavailability remain insufficiently characterized. Accordingly, this review does not propose T. buceras as a preventive or therapeutic intervention and does not claim superiority over better-characterized medicinal plants. Instead, this review critically synthesizes published species-specific chemical and biological findings and evaluates their methodological limitations. The direct retinal evidence supports partial cytoprotection in an ARPE-19 oxidative-injury model, whereas the non-retinal inflammatory findings concern different preparations and experimental systems. Chemical characterization, cellular responses, and contextual mechanistic evidence are, therefore, considered separately. The available findings do not establish a disease-modifying effect on dAMD, clinically achievable retinal exposure, or chronic ocular safety.