Abstract

We aimed to investigate the antioxidant and acetylcholinesterase inhibitory activities of the anthocyanin rich extract of grape skin. Grape skin anthocyanin (GSA) neutralized free radicals in different test systems, such as 2,-2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays, to form complexes with Fe2+ preventing 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced erythrocyte hemolysis and oxidative DNA damage. Moreover, GSA decreased reactive oxygen species (ROS) generation in isolated mitochondria thus inhibiting 2',-7'-dichlorofluorescin (DCFH) oxidation. In an in vivo study, female BALB/c mice were administered GSA, at 12.5, 25, and 50 mg per kg per day orally for 30 consecutive days. Herein, we demonstrate that GSA administration significantly elevated the level of antioxidant enzymes in mice sera, livers, and brains. Furthermore, GSA inhibited acetylcholinesterase (AChE) in the in vitro assay with an IC50 value of 363.61 ”g/mL. Therefore, GSA could be an excellent source of antioxidants and its inhibition of cholinesterase is of interest with regard to neurodegenerative disorders such as Alzheimer’s disease.

Highlights

  • Free radicals or reactive oxygen species (ROS) play many important roles in physiological and pathological processes

  • Grape skin anthocyanin (GSA) could be an excellent source of antioxidants and its inhibition of cholinesterase is of interest with regard to neurodegenerative disorders such as Alzheimer’s disease

  • The IC50 value of vitamin C was 71.50 ÎŒg/mL. These results indicate that GSA might act as an electron or hydrogen donator to scavenge DPPH radicals

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Summary

Introduction

Free radicals or reactive oxygen species (ROS) play many important roles in physiological and pathological processes. Oxidative stress is a biological phenomenon that results from a biochemical imbalance between the formation and clearance/buffering of free radicals [1]. Mitochondria are the major source of cellular ROS. The accumulation of ROS induces oxidative damage of mitochondrial. DNA (mtDNA), proteins, and lipids, and has been shown to contribute to the decline in physiological function of cells resulting in a variety of diseases and accelerated aging [2]. Enzymatic systems in cells and body fluids regulate the level of ROS, which otherwise might generate a cascade of products and lead to assailing oxidants. Antioxidant enzymes modulate the activities of these ROS and play a role in vascular function [4]

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