# Resveratrol: A Review on the Biological Activity and Applications
## 9 Antioxidant Effect  
RSV is a well-known natural compound active as a scavenger of free radicals. In several in vitro antioxidant assays, such as 2,2\({}^{\prime}\)-azino-_bis_(3-ethylbenzothazoline)-6-sulfonic acid (ABTS), 2,2-diphenyl-1-picrylhydrazyl (DPPH), \(N\),_N_-dimethyl-_p_-phenylenediamine(DMPD), H\({}_{2}\)O\({}_{2}\), NO, oxygen radical absorbance capacity (ORAC), total antioxidant activity (TAC), cupric reducing antioxidant capacity (CUPRAC), ferric reducing antioxidant power (FRAP), RSV exhibited radical scavenging, reducing power, Cu\({}^{2+}\) and Fe\({}^{2+}\) chelating effects. Also, RSV induces an inhibition of lipid peroxidation of linoleic acid emulsion greater than \(\alpha\)-tocopherol, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox), butylated hydroxytoluene (BHT), and butylated hydroxyanisole (BHA) [189; 190; 191].  
RSV has in vitro and in vivo antioxidant effects, both directly and indirectly, by the inhibition of ROS production and modulation of several antioxidant enzymatic systems, respectively [192; 193].  
Nanoencapsulation using soy lecithin/sugar esters, Tween 20/glycerol monooleate, Tween 80/dodecanol (Dod), and Span 80/Dod preserved physicochemical stability and in vitro antioxidant capacity of fRSV as shown in chemical (DPPH, ABTS) and cellular assays (Caco-2 line), comparing with dimethyl sulfoxide (DMSO)-solubilized unencapsulated \(t\)RSV [194; 195].  
RSV is a powerful natural antioxidant and an extremely photosensitive compound. Moreover, after oral administration, RSV has low bioavailability due to its low solubility and rapid first-pass effect [196; 197]. In this regard, the chemical stability, oral bioavailability, and antioxidant potential of \(t\)RSV were improved using both lipid-coated nanocrystals [198] and an electrospun nanofiber system based on polyvinylpyrrolidone (PVP) and hydroxypropyl-\(\beta\)-cyclodextrintrim (HP\(\beta\)CD) [199].  
RSV has been determined to defend LDLs against peroxididative degeneration. Being a tyrosine kinase suppressor, it also has the capacity to inhibit intracellular adhesion molecule \(1\) and vascular cell adhesion molecule \(1\) expression and to stop the attachment of monocytes and granulocytes to endothelial cells. This mechanism is autonomous from its antioxidant action and provides a different interpretation [200].  
Nutritional addition of RSV inhibits lipid peroxidation, the critical consequence of oxidative stress caused by chronic ethanol treatment. During a study on ethanol-treated rats, RSV substantially counteracted the elevation in MDA, a marker of oxidative damage, concentrations in the liver, heart, brain, and testes, demonstrating its protective effect [201]. Numerous assays evaluated the inhibitory effect of RSV in oxidative stress. However, the association of RSV and vitamins C and E is more efficient in protecting the cells than any of these antioxidants alone [202].  
In a randomized clinical trial on older adults with T2D, RSV treatment, 1000 mg/day for six months, exhibited a statistically significant antioxidant effect highlighted by the decreasing of oxidative stress biomarkers and increasing of TAC and SIRT1 levels [203].