Unveiling protective mechanisms of wild olive (acebuche) oil in retinal pigment epithelial cells with hypertensive phenotype

• DOI: 10.1113/jp287367
• Publication Date: 2025-03-11T22:45:34Z
• Authors: Álvaro Santana‐Ga...; Claudia Reyes‐Goya; Pablo Espinosa‐Ma...; Rosa M. Troya‐Toledo; Helder André; Alfonso Mate; Carmen M. Vázquez

AbstractArterial hypertension leads to oxidative and inflammatory imbalances, triggering hypertensive organ damage through several pathways. We have previously described the antioxidant and anti‐inflammatory properties of olive oil extracted from the wild olive tree (Olea europaea var. sylvestris, acebuche, ACE) against hypertensive ocular damage. The aim of this study was to clarify the molecular mechanisms involved in the beneficial effect of ACE oil on hypertensive eyes, focusing on nitric oxide (NO)/arginine metabolism. To this end, we used retinal pigment epithelial cells (ARPE19) treated with angiotensin II as a hypertensive‐like model. These cells were also incubated with extracellular vesicles (EVs) isolated from animals fed diets enriched in either ACE oil or extra virgin olive oil (EVOO), with the latter serving as a reference oil for comparison. Our results showed that circulating ACE oil‐ and EVOO‐derived EVs can modulate the production of reactive oxygen species by both NADPH oxidase and mitochondria, the activity and expression of l‐arginine transporter CAT‐1, angiotensin AT1 and AT2 receptors, and arginases, as well as the levels of NO and asymmetric dimethylarginine. Our findings demonstrate that: (1) changes in NO metabolism are involved in the protective effects of wild olive oil against hypertension‐related ocular oxidative stress, and (2) these modifications appear to be mediated by EVs. imageKey points l‐Arginine transport contributes to the beneficial effect of wild olive oil on the eyes of hypertensive mice. Extravesicular vesicles from wild olive oil (ACE‐EVs) prevent changes in nitric oxide (metabolism in hypertensive‐like retinal pigment epithelial cells. Reactive oxygen species produced by both NADPH oxidase and mitochondria can be mitigated by ACE‐EV treatment.