Along-Path Evolution of Biogeochemical and Carbonate System Properties in the Intermediate Water of the Western Mediterranean

A basin-scale oceanographic cruise (OCEANCERTAIN2015) was carried out in the Western Mediterranean (WMED) in summer 2015 to study the evolution of hydrological and biogeochemical properties of the most ubiquitous water mass of the Mediterranean Sea, the Intermediate Water (IW). IW is a relatively warm water mass, formed in the Eastern Mediterranean (EMED) and identified by a salinity maximum all over the basin. While it flows westward, toward and across the WMED, it gradually loses its characteristics. This study describes the along-path changes of thermohaline and biogeochemical properties of the IW in the WMED, trying to discriminate changes induced by mixing and changes induced by interior biogeochemical processes. In the first part of the path (from the Sicily Channel to the Tyrrhenian Sea), respiration in the IW interior was found to have a dominant role in determining its biogeochemical evolution. Afterward, when IW crosses regions of enhanced vertical dynamics (Ligurian Sea, Gulf of Lion and Catalan Sea), mixing with surrounding water masses becomes the primary process. In the final part of the investigated IW path (the Menorca-Mallorca region), the role of respiration is further masked by the effects of a complex circulation of IW, indicating that short-term sub-regional hydrological processes are important to define IW characteristics in the westernmost part of the investigated area. A pronounced along-path acidification was detected in IW, mainly due to remineralization of organic matter. This induced a shift of the carbonate equilibrium toward more acidic species and makes this water mass increasingly less adequate for an optimal growth of calcifying organisms. The carbonate buffering capacity also decreases as IW flows through the WMED, making it more exposed to the adverse effects of a decreasing pH. The present analysis indicates that IW evolution in the sub-basins of the WMED is currently driven by complex hydrological and biogeochemical processes, which could be differently impacted by coming climate changes, in particular considering expected increases of extreme meteorological events, mainly due to the warming of the Mediterranean basin

Apricot melanoidins prevent oxidative endothelial cell death by counteracting mitochondrial oxidation and membrane depolarization

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

The carbonate chemistry of the Western Mediterranean during the OCEAN CERTAIN 2015 cruise

In Summer 2015 (4-31 August), CNR-ISMAR carried out an oceanographic field-study in the Western Mediterranean Sea, on board of R/V MINERVA UNO. Sampling stations consisted in 7 transects, that spanned from Sicily Channel to Ligurian sea, Catalan sea, and Balearic Basin, dividing the area in sub-basins. 92 stations were visited totally. The dataset includes 550 discrete data of carbonate chemistry (pH-total scale and Total Alkalinity), concentrations of dissolved oxygen, and basic hydrological data (temperature, salinity and density). Methods: At each station, pressure (dbar), temperature (°C), and conductivity(mS/cm) were measured with a CTD SBE 911 plus General Oceanics Rosette System, equipped with 24 12-litres Niskin Bottles. Salinity (S, psu) and depth (m) were calculated by Sea-Bird Scientific routines. Seawater samples (n = 550) for the determination of biogeochemical parameters were collected from the Niskin bottles. Samples for dissolved oxygen (DO) were drawn in 60-mL BOD bottles and treated with Winkler reagents immediately after collection. For the determination of pH on the total hydrogen ion scale at 25 °C (pHT25), the samples were drawn after DO samples into 10 cm long cylindrical glass cells and analyzed spectrophotometrically. For the determination of total alkalinity (TA; μmol kg-1), the samples were collected in 300 ml borosilicate bottles, poisoned with mercuric chloride, tightly closed and stored in the dark at a temperature similar to the in situ one (4-25 °C). DO samples were analyzed by the Winkler method (Grasshoff et al., 1999) using an automated Metrohm 798 MPT Titrino potentiometric titration system (CV = 0.17 % at 210 µmol L-1). pHT25 was measured on board, within 24 h after the sampling, using the spectrophotometric method with m-cresol purple as indicator (Clayton and Byrne, 1993). The precision was ±0.002 units (n = 3), accuracy and stability of the method were checked daily with reference seawater certified for TA and TCO2 (n = 34, CRM batch 146 provided by Prof A. G. Dickson, Scripps, 210 California). TA was determined by potentiometric titration in an open cell with a difference derivative readout (Hernandez-Ayon et al., 1999). The average precision was ±2.0 μmol kg-1 (n = 86 duplicate samples) and the accuracy was checked daily by the titration of certified reference seawater (n = 59, CRM batch 146

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

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

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

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

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

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

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