Identification of Oxidation Compounds of 1‑Stearoyl-2-linoleoyl-<i>sn</i>-glycero-3-phosphoethanolamine during Thermal Oxidation

Heat-induced oxidative modification of phosphatidylethanolamine molecular species as potential functional food components was investigated. 1-Stearoyl-2-linoleoyl-<i>sn</i>-glycero-3-phosphoethanolamine (SLPE) was chosen as a model. The optimal temperature for hydroperoxide formation was determined by mass spectrometry. The maximal level of formation of this compound was obtained at 125 °C. The structures of nonvolatile organic compounds (non-VOCs) were identified using liquid chromatography–electrospray ionization mass spectrometry combined with an acid treatment. Kinetics of formation of non-VOCs was monitored over time. Results showed that the level of the SLPE precursor rapidly decreased during thermal oxidation and oxygenated products, such as hydroxyl, oxo, or epoxy groups, were formed. The VOCs formed from oxidized SLPE were determined by headspace solid-phase microextraction followed by gas chromatography–mass spectrometry analysis. The result showed that a saturated methyl ketone (2-heptanone) was the most predominant VOC of SLPE. Kinetics indicated that the formation of VOCs was related not only to the decomposition of hydroperoxides but also to the further decomposition of non-VOCs

Comparison of the Volatiles Formed by Oxidation of Phosphatidylcholine to Triglyceride in Model Systems

The oxidative stability of oleoyl and linoleoyl residues esterified in the form of triglyceride (TAG) and phosphatidylcholine (PC) during thermal treatment was investigated. Headspace solid-phase microextraction (HS-SPME) followed by gas chromatography–mass spectrometry (GC–MS) analysis was used to determine the volatile compounds from oxidized PL and TAG molecular species. The results showed that aldehydes were the major volatile oxidized compounds (VOCs) of 1-stearoyl-2-oleoyl-<i>sn</i>-glycero-3-phosphocholine (SOPC), 1-stearoyl-2-linoleoyl-<i>sn</i>-glycero-3-phosphocholine (SLPC), and 1,3-distearoyl-2-linoleoyl-glycerol (SLS), while ketones, especially saturated methyl ketones, were the major VOCs of 1,3-distearoyl-2-oleoyl-glycerol (SOS). The monitoring of the oxidative degradation using liquid chromatography–electrospray ionization–mass spectrometry (LC–ESI–MS) showed that either monounsaturated or diunsaturated fatty acyl groups were less oxidized when in the form of PCs than when in the form of TAGs. This finding demonstrated that the choline group in the form of PCs could increase the stability of fatty acyl groups to oxidation in comparison to TAGs

Investigation of Biomarkers of Bile Tolerance in <i>Lactobacillus casei</i> Using Comparative Proteomics

The identification of cell determinants involved in probiotic features is a challenge in current probiotic research. In this work, markers of bile tolerance in <i>Lactobacillus casei</i> were investigated using comparative proteomics. Six <i>L. casei</i> strains were classified on the basis of their ability to grow in the presence of bile salts in vitro. Constitutive differences between whole cell proteomes of the most tolerant strain (<i>L. casei</i> Rosell-215), the most sensitive one (<i>L. casei</i> ATCC 334), and a moderately tolerant strain (<i>L. casei</i> DN-114 001) were investigated. The ascertained subproteome was further studied for the six strains in both standard and bile stressing conditions. Focus was on proteins whose expression levels were correlated with observed levels of bile tolerance in vitro, particularly those previously reported to be involved in the bile tolerance process of lactobacilli. Analysis revealed that 12 proteins involved in membrane modification (NagA, NagB, and RmlC), cell protection and detoxification (ClpL and OpuA), as well as central metabolism (Eno, GndA, Pgm, Pta, Pyk, Rp1l, and ThRS) were likely to be key determinants of bile tolerance in <i>L. casei</i> and may serve as potential biomarkers for phenotyping or screening purposes. The approach used enabled the correlation of expression levels of particular proteins with a specific probiotic trait

SCD1 expression in ALS patient muscle and after nerve injury.

<p>(A) Expression of SCD1 and SCD5 in deltoid muscle biopsies from ALS patients and healthy subjects (CT, white columns), as identified by microarray analysis of the database deposited at <a href="http://www.ebi.ac.uk/arrayexpress/(accession" target="_blank">http://www.ebi.ac.uk/arrayexpress/(accession</a> number E-MEXP-3260) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0064525#pone.0064525-Pradat1" target="_blank">[12]</a>. ALS samples were obtained from muscle not clinically or electromyography affected (Unaff, orange columns) and from muscle with advanced pathology, characterized by reduced strength and neurogenic electromyography pattern (Aff, brown columns). *<i>P</i><0.05 (1-way ANOVA followed by Tukey's multiple comparison test, n = 4–10). (B) Expression of SCD1 in gastrocnemius following sciatic nerve axotomy (Axo) or crush at indicated post-operation days. Contralateral muscle expression is represented by 100% baseline. **<i>P</i><0.01, ***<i>P</i><0.001 (One sample t-test, n = 4–10).</p

Gene expression specific to the motor end plate in SCD1 knockout mice.

<p>Expression of AChR-α, AChR-γ, AChR-ε and MuSK in gastrocnemius and tibialis anterior from SCD1 knockout mice (brown columns) and wild-type littermates (white columns). *<i>P</i><0.05, ***<i>P</i><0.001 (Unpaired t-test, n = 4–11).</p

Muscle function recovery in SCD-deficient mice submitted to nerve crush.

<p>Restoration of muscle grip strength in SCD1 knockout mice (A) or MF-438 treated mice (C) (black circles) and corresponding control littermates (white circles) at the indicated post-operation times. ***<i>P</i><0.001 (2-way ANOVA, n = 4–12). Percentage of electromyography episodes of spontaneous activity in SCD1 knockout mice (Inset A) or MF-438 treated mice (Inset C) (KO or MF, brown columns) and corresponding control littermates (WT or CT, white columns) two weeks after sciatic nerve crush. *<i>P</i><0.05 (Unpaired t-test, n = 4–7). (B) Relative density of muscle fiber types in ipsilateral and contralateral tibialis anterior from SCD1 knockout mice and wild-type littermates two weeks after sciatic nerve crush. According to SDH histochemistry, fibers were classified as dark brown colored fibers with high metabolic oxidative capacity (brown columns), pale brown colored fibers with medium oxidative capacity (orange columns) and non-satined fibers (white columns). *<i>P</i><0.05 and ***<i>P</i><0.001 (1-way ANOVA followed by Tukey's multiple comparison test, (n = 4–6). (D) Kaplan-Meier curves showing the percentage of MF-438 treated mice (black circles) and control littermates (white circles) that started to exhibit a grip strength distinct from zero after initial total paralysis. Logrank test (n = 10–11). Inset D, averaged time at start of recovery in MF-438 treated mice (MF, brown column) and control littermates (CT, white column). *<i>P</i><0.05 (Unpaired t-test, n = 10–11).</p

Effects of MF-438 on metabolism and muscle function.

<p>(A) C16:1/C16:0 and C18:1/C18:0 fatty acid ratio in plasma from MF-438 treated mice (brown columns) and control littermates (CT, white columns). ***<i>P</i><0.001 (Unpaired t-test, n = 4–6). (B) Time course of respiratory quotient (RQ) before and after treatment with MF-438 at a dose of 10 mg/kg body mass/day (indicated by the black bar) (n = 4). Time course of body mass (C), muscle grip strength expressed as a percentage of day 0 (D), and specific grip strength, as determined by normalizing peak force to body mass (E), in mice fed regular chow (white circles) and mice fed regular chow supplemented with MF-438 (black circles). **<i>P</i><0.01 (2-way ANOVA followed by Bonferroni test, n = 5–6). (F) Expression of PGC1-α, AChR-α, and MuSK in gastrocnemius from MF-438 treated mice (brown columns) and control littermates (white columns). *<i>P</i><0.05 (Unpaired t-test, n = 3–9).</p

MOESM2 of Beneficial effects of cherry consumption as a dietary intervention for metabolic, hepatic and vascular complications in type 2 diabetic rats

Additional file 2: Figure S1. Impact of cherry consumption on pancreatic oxidative stress 4 months into the experimental period. Oxidative stress is assessed by dihydroethidine fluorescent probe (DHE) after 4 months of normal diet (ND), high fat high fructose (HFHF) diet, HFHF 2 months + ND 2 months (HFHF/ND), HFHF 2 months + ND with cherry supplementation 2 months (HFHF/NDCherry) and HFHF 2 months + HFHF with cherry supplementation 2 months groups (HFHFCherry). Bar scale = 100. All the results are shown as the mean ± SEM of 6 different experiments. Asterisk represents significant results vs. ND; $ vs. HFHF

Metabolic phenotype of muscle from SCD1 knockout mice.

<p>(A) Expression of PGC1-α, PPARα and PDK4 in gastrocnemius and tibialis anterior from SCD1 knockout mice (brown columns) and wild-type littermates (white columns). *<i>P</i><0.05, **<i>P</i><0.01 (Unpaired t-test, n = 3–11). (B) Number of muscle fibers in tibialis anterior from SCD1 knockout mice (KO, brown column) and wild-type littermates (WT, white column). *<i>P</i><0.05 (Unpaired t-test, n = 7–10). (C) Distribution of the calibers of muscle fibers in tibialis anterior from SCD1 knockout mice (327 fibers, black circles) and wild-type littermates (283 fibers, white circles). Representative microphotographs of wild-type and knockout tibialis anterior are shown. (D) Averaged cross-sectional area of SDH-positive and SDH-negative fibers in tibialis anterior from SCD1 knockout mice (brown columns) and wild-type littermates (white columns). *<i>P</i><0.05, **<i>P</i><0.01 (Unpaired t-test, n = 7–10). (E) Number of SDH-positive (orange bars) and SDH-negative fibers (white bars) in tibialis anterior from SCD1 knockout mice (KO) and wild-type littermates (WT). ***<i>P</i><0.001 (Chi-square test, n = 283–327).</p

SCD indices are higher in ALS patients than in control subjects.

<p>(A) Palmitoleate to palmitate ratio (16:1/16:0) in serum and blood cells from ALS patients (ALS) and control subjects (CT). (B) Oleate to stearate ratio (18:1/18:0) in serum and blood cells from ALS patients (ALS) and control subjects (CT). *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001 (Mann-Withney test, n = 48).</p