Uric acid (UA), a key purine metabolite associated with metabolic, cardiovascular, and renal disorders, has been extensively investigated using electrochemical sensors. Increasing efforts now focus on translating these technologies into commercial point-of-care (POC) platforms for rapid, decentralized detection. Commercial screen-printed electrodes (SPEs) are widely employed as substrates for such platforms, typically after surface modification with nanomaterials or recognition elements; however, their inherent, unmodified analytical capabilities remain largely uncharacterized. This gap is significant, as the baseline performance of the underlying electrode ultimately constrains or enables the benefits of any subsequent modification. Here, we systematically compare two commercially available SPEs, DRP-110 and DRP-150, for UA detection using differential pulse voltammetry under standardized conditions. Both electrodes exhibited two distinct UA oxidation peaks. The first peak gave linear calibration over 0.02–0.5 µM (R² = 0.9863 DRP-110, 0.9928 DRP-150), with validated LOD/LOQ of 0.076/0.230 µM (DRP-110) and 0.055/0.166 µM (DRP-150); the second peak extended the linear working range to 1–1000 µM (DRP-110, R² = 0.9833) and 1–2000 µM (DRP-150, R² = 0.9928), with LOD/LOQ of 3.37/10.20 µM and 2.23/6.77 µM, respectively, derived from its low-concentration segment. DRP-150 demonstrated superior sensitivity at both peaks. However, both electrodes showed low selectivity toward ascorbic acid. Spike recovery testing in modified artificial urine gave recoveries of 68.0–98.49%, supporting preliminary feasibility in a defined urine-like matrix.

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, with aging as one of its main risk factors. Cellular senescence and oxidative stress form a bidirectional vicious cycle that drives vascular aging, endothelial dysfunction, and atherosclerotic progression. This state-of-the-art review synthesizes current evidence on the interplay between oxidative stress and senescence in cardiovascular aging and critically assesses whether antioxidant strategies can benefit vascular health. A targeted literature search was conducted in PubMed/MEDLINE, Web of Science, and Scopus (2016–2026). While endogenous antioxidant defenses decline with age, exogenous antioxidants, including resveratrol, vitamins C and E, omega-3 fatty acids, carotenoids, and coenzyme Q10,demonstrate promising preclinical effects, yet large-scale clinical trials have yielded inconsistent results. The VITAL and STRENGTH trials failed to demonstrate significant cardiovascular benefit with omega-3 supplementation, and elevated serum β-carotene was found paradoxically associated with increased cardiovascular mortality. Emerging mitochondria-targeted antioxidants (MitoQ, MitoTEMPO) show preclinical promise but require further clinical validation. Current evidence does not support antioxidant supplementation for cardiovascular prevention. Lifestyle interventions, particularly antioxidant-rich dietary patterns such as the Mediterranean diet, remain the safest strategy. Future research should develop personalized approaches guided by oxidative stress biomarkers and long-term trials.