Resveratrol (2005, 2017) & Macular Degeneration
Learn more about macular degeneration recommendations
Scientists report that resveratrol, taken orally, shows up in blood samples within 10 minutes of ingestion and is able to cross the semi-permeable blood-brain and blood-ocular barriers making it a valuable micronutrient for ocular conditions such as macular degeneration.
Researchers measured the trans-resveratrol (and its metabolites) concentrations in human eyes.
The researchers noted that the antioxidant, anti-inflammatory agent abilities of resveratrol, along with its capacity to inhibit formation of extra blood vessels make it valuable as a nutrient for macular degeneration.
Scientists determined that trans-resveratrol and three metabolites of resveratrol (especially resveratrol-3-O-sulfate) were found in eye tissue ) after taking dosages orally. Theese measurements help to define dosages in future treatment of ocular disease.
Researchers: S. Wang, Z. Wang, et al,
Published: Tissue Distribution of trans-Resveratrol and Its Metabolites after Oral Administration in Human Eyes, Journal of Ophthalmology, March, 2017.
Researchers have found that moderate wine drinking and antioxidant-rich diets may decrease risk of age-related macular degeneration. Development of this and other retinal conditions, such as proliferative vitreoretinopathy (PVR), is associated with oxidative stress in the retinal pigment epithelium (RPE), where the health of the retina is maintained by providing structural and nutritional support.
The researchers indicate that resveratrol, a red wine polyphenol, may be responsible, in part, for these health benefits. To test this hypothesis, the antioxidant and antiproliferative effects of resveratrol were examined in a human RPE cell line (designated ARPE-19). The results suggest that resveratrol can reduce oxidative stress and hyperproliferation of the RPE.
Researchers: R.E. King, K.D. Kent, et al,
Published: Resveratrol reduces oxidation and proliferation of human retinal pigment epithelial cells via extracellular signal-regulated kinase inhibition, Chemico-Biological Interacttions, January, 2005.