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Apricot Melanoidins Prevent Oxidative Endothelial Cell Death by Counteracting Mitochondrial Oxidation and Membrane Depolarization
Author(s) -
Annalisa Cossu,
Anna Maria Posadino,
Roberta Giordo,
Costanza Emanueli,
Anna Maria Sanguinetti,
Amalia Piscopo,
Marco Poiana,
Giampiero Capobianco,
Antonio Piga,
Gianfranco Pintus
Publication year - 2012
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0048817
Subject(s) - hydrogen peroxide , oxidative stress , mitochondrion , depolarization , reactive oxygen species , programmed cell death , chemistry , oxidative phosphorylation , biochemistry , membrane potential , browning , intracellular , biophysics , microbiology and biotechnology , biology , apoptosis
The cardiovascular benefits associated with diets rich in fruit and vegetables are thought to be due to phytochemicals contained in fresh plant material. However, whether processed plant foods provide the same benefits as unprocessed ones is an open question. Melanoidins from heat-processed apricots were isolated and their presence confirmed by colorimetric analysis and browning index. Oxidative injury of endothelial cells (ECs) is the key step for the onset and progression of cardiovascular diseases (CVD), therefore the potential protective effect of apricot melanoidins on hydrogen peroxide-induced oxidative mitochondrial damage and cell death was explored in human ECs. The redox state of cytoplasmic and mitochondrial compartments was detected by using the redox-sensitive, fluorescent protein (roGFP), while the mitochondrial membrane potential (MMP) was assessed with the fluorescent dye, JC-1. ECs exposure to hydrogen peroxide, dose-dependently induced mitochondrial and cytoplasmic oxidation. Additionally detected hydrogen peroxide-induced phenomena were MMP dissipation and ECs death. Pretreatment of ECs with apricot melanoidins, significantly counteracted and ultimately abolished hydrogen peroxide-induced intracellular oxidation, mitochondrial depolarization and cell death. In this regard, our current results clearly indicate that melanoidins derived from heat-processed apricots, protect human ECs against oxidative stress.

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