Oxidative stress plays a critical role in the development of chronic ocular conditions including cataracts, age-related macular degeneration, and diabetic retinopathy. There is a need to explore the potential of topical antioxidants to slow the progression of those conditions by mediating oxidative stress and maintaining ocular health. Selenium has attracted considerable attention because it is a component of selenoproteins and antioxidant enzymes. The application of selenium to a patient can increase selenoprotein expression, counteracting the effect of reactive oxygen species by increasing the presence of antioxidant enzymes, and thus slowing the progression of chronic ocular disorders. Oxidative stress effects at the biomolecular level for prevalent ocular conditions are described in this review along with some of the known defensive mechanisms, with a focus on selenoproteins. The importance of selenium in the eye is described, along with a discussion of selenium studies and uses. Selenium’s antioxidant and anti-inflammatory qualities may prevent or delay eye diseases. Recent breakthroughs in drug delivery methods and nanotechnology for selenium-based ocular medication delivery are enumerated. Different types of selenium may be employed in formulations aimed at managing ocular oxidative stress conditions.

Background/Objectives: Oxidative stress plays a critical role in the development of ocular diseases such as cataracts. Selenium nanoparticles (SeNPs) offer antioxidant benefits with low toxicity. This study aimed to evaluate the antioxidant activity of SeNPs coated with D-α-tocopheryl polyethylene glycol succinate (TPGS) in human lens epithelial (HLE) cells. Methods: SeNPs were synthesised by reducing sodium selenite with ascorbic acid in the presence of TPGS. Physicochemical characterisation was carried out using dynamic light scattering to assess size and surface charge. Antioxidant activity was measured by a 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay. Cytocompatibility was assessed on adult retinal pigment epithelial (ARPE-19) and HLE cells using PrestoBlue. Functional antioxidant performance was determined through enzymatic assays for glutathione peroxidase (GPx), thioredoxin reductase (TrxR), and glutathione (GSH), and lipid peroxidation was assessed using malondialdehyde (MDA) quantification. Catalase mimicry was evaluated under 3-amino-1,2,4-triazole (3-AT)-induced inhibition. Results: The optimal SeNP formulation had an average hydrodynamic diameter of 44 ± 3 nm, low PDI (<0.1), and a surface charge of −15 ± 3 mV. These TPGS-SeNPs demonstrated strong radical scavenging (EC₅₀ ≈ 1.55 µg/mL) and were well tolerated by ARPE-19 cells (IC₅₀ = 524 µg/mL), whereas HLE cells had a narrower biocompatibility window (≤0.4 µg/mL, IC₅₀ = 2.2 µg/mL). Under oxidative stress, SeNPs significantly enhanced GPx and TrxR activity but did not affect GSH or MDA levels. No catalase-mimetic activity was observed. Conclusions: TPGS-SeNPs exhibit potent antioxidant enzyme modulation under stress conditions in HLE cells. Although not affecting all oxidative markers, these nanoparticles show promise for non-invasive strategies targeting lens-associated oxidative damage, including cataract prevention.

Arteriovenous grafts are widely used for hemodialysis access, yet high failure rates remain a major clinical challenge. Decellularized blood vessels offer promising alternatives, but effective protocols must remove cellular and antigenic components while preserving extracellular matrix (ECM) integrity. This is particularly challenging in elastic arteries, where smooth muscle cells are anchored by dense actin filaments that are difficult to remove without ECM damage from harsh treatments. Here, we present a decellularization strategy based on actin-disrupting agents, specifically Latrunculin B, to facilitate removal of these dense cytoskeletal structures. The protocol integrates osmotic shock, high-ionic-strength salts, and Triton X-100 within a shortened processing time. Full-length porcine carotid arteries were decellularized using a dual-flow perfusion system, and five protocols were evaluated for removal of nuclear and immunogenic material, ECM preservation, mechanical properties, and cytocompatibility with human endothelial cells (HUVECs). All protocols substantially reduced nuclear material while preserving elastin, collagen, and mechanical integrity. Complete removal of immunogenic proteins was achieved with a final alkaline Triton X-100 wash (pH 8–14), highlighting the effectiveness of alkaline treatment in solubilizing membrane-bound antigens. All scaffolds supported HUVEC adhesion and formed a confluent endothelial monolayer within 8 days. Overall, integrating actin disruption via Latrunculin B with dual-salt–Triton processing, alkaline washing, and perfusion enhances decellularization efficiency, preserves ECM structure, reduces processing time and cost, and yields cytocompatible small-diameter vascular scaffolds with strong translational potential.