Electropherograms of (1) 0.5 mmol/L EG, (2) 0.750 mmol/L human serum albumin (HSA) and (3) mix of 0.5 mmol/L EGCG and 0.750 mmol/L human serum albumin (HSA) monitored at 280 nm.

<p>Electropherograms of (1) 0.5 mmol/L EG, (2) 0.750 mmol/L human serum albumin (HSA) and (3) mix of 0.5 mmol/L EGCG and 0.750 mmol/L human serum albumin (HSA) monitored at 280 nm.</p

Comparison between the stabilizing effect of HCl, cysteine and human serum albumin on EGCG.

<p>0.5 mmol/L of catechin was separately incubated at 25°C for 48 h with only PBS, 10 mmol/L of cysteine in PBS, 50 mmol/L of HCl, 10 mmol/L of cysteine in 50 mmol/L HCl, or 0.750 mmol/L of Human Serum Albumin (HSA) in PBS. During the incubation period, 200 μL of the mixture has been taken at different time points (8h, 24 h and 48 h), mixed with 100 μL of acetonitrile and centrifuged to precipitate HSA. The resulting supernatant has been directly injected on capillary electrophoresis UV detection to evaluate residual catechin. The time-points associated this symbol (★) are significantly different from each other; the time-points associated this symbol (◆) are significantly different from each other; the time-points associated this symbol (■) are significantly different from each other; the time-points associated this symbol (❖) are significantly different from each other.</p

Melanoidins protect endothelial cells from hydrogen peroxide-induced mitochondrial damage and cell death.

<p>Dose-dependent effect of melanoidins on hydrogen peroxide (H₂O₂)-induced (A) cell death, (B) mitochondrial metabolic activity and (C) mitochondrial membrane potential. Data are the mean ± SE of four experiments. (A–C) *, significantly different from the control.</p

ECV304 cells lines constitutively expressing the cytoplasmic (cyto-roGFP) and mitochondrial (mito-roGFP) form of roGFP.

<p>Cells were grown in glass chamber slides at concentrations to allow 50–70% confluence in 24 hrs. On the day of experiments, cells were washed with PBS three times, counterstained with the mitochondrial marker MitoTracker Red and the nuclear marker <b><i>Hoechst</i></b>, fixed with 4% paraformaldehyde and mounted for fluorescence microscopy visualization. Images (A) and (C) depict respectively merged photos of ECV304 cells expressing the cyto-and mito-<i>roGFP</i> (green) protein, <b><i>Hoechst</i></b> staining (blue) and bright-field (40X, NA = 1.00). Images (B) and (D) depict respectively merged photos of ECV304 cells expressing the cyto-and mito-<i>roGFP</i> (green) protein, counterstained with <b><i>Hoechst</i></b> (blue) (100X, NA = 1.35)). The <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048817#pone-0048817-g005" target="_blank">figure 5F</a>, depicts the merged photo of ECV304 cells expressing the mito-roGFP protein (D) and ECV304 cells stained with the mitochondrial marker MitoTracker Red (E). (100X, NA = 1,35)).</p

Hydrogen peroxide induces mitochondrial damage and cell death.

<p>Dose-dependent effect of hydrogen peroxide (H₂O₂) on (A) cell viability, (B) mitochondrial metabolic activity and (C) mitochondrial membrane potential. Data are the mean ± SE of four experiments. (A–C) *, significantly different from the control.</p

Hydrogen peroxide induces oxidation of both cytosolic and mitochondrial compartments.

<p>Dose-dependent effect of hydrogen peroxide (H₂O₂) on mitochondrial (mito-roGFP) and cytoplasmic (cyto-roGFP) ro-GFP oxidation. Data are the mean ± SE of four experiments. (A–B) *, significantly different from the control.</p

Melanoidins protect human endothelial cells from hydrogen peroxide-induced intracellular oxidative stress.

<p>Dose-dependent effect of melanoidins on H₂O₂-induced cytoplasmic (cyto-roGFP) and mitochondrial (mito-roGFP) roGFP oxidation. Data are the mean ± SE of four experiments. (A–B) *, significantly different from the control.</p

Cytoprotective, antioxidant, and anti-migratory activity of <i>Pistacia lentiscus L</i>. supercritical carbon dioxide extract on primary human endothelial cells

Green chemistry is a useful tool for producing valuable chemicals from biomass. However, extracted compounds need to be tested for safety and efficacy before their use in humans. Here we investigate the chemical composition and biological effects of a leaves Pistacia lentiscus L. supercritical carbon dioxide (SCCO2) extract. Terpenes represented the main extract fraction, with Germacrene D (11.18%), delta-cadinene (10.54%), and alpha-pinene (8.7%) the most abundant molecules. Challenged with endothelial cells (ECs), increasing extract concentrations failed to affect cell proliferation or promote cell toxicity. ROS assessment in unstressed and H2O2-treated ECs revealed an extract dose-dependent antioxidant activity. Exposition of H2O2-treated ECs to increasing extract concentrations dose-dependently counteracted H2O2-induced cell impairments. The extract significantly counteracted fetal calf serum-induced ECs migration. For the first time, we report that a SCCO2 extract obtained from PL leaves is safe on ECs and may be a useful source of valuable compounds with vasculoprotective properties.</p

Apricots melanoidins are not toxic for endothelial cells.

<p>Effect of different concentrations of melanoidins on (A) cell viability and (B) mitochondrial metabolic activity. Data are the mean ± SE of four experiments.</p

Changes in chemical parameters elicited by fruit processing.

<p>(A) Changes in antioxidant activity and color expressed as hue variation (tan - 1 b*/a*). (B) Changes in color expressed as hue variation (tan - 1 b*/a*). (C) Changes in color expressed as browning index (Abs at 420 nm g⁻¹ dm of fruit). Fresh, fresh fruits; M, melanoidins; B, blanching. Data are the mean ± SE from four or five measurements. (A–C) a; b, significantly different from the fresh sample.</p