Perfluorooctanoic Acid-Disturbed Serum and Liver Lipidome in C57BL/6 Mice.

Perfluorooctanoic acid is a manufactured material extensively utilized in industrial and consumer products. As a persistent organic pollutant, perfluorooctanoic acid has raised increasing public health concerns recently. Although perfluorooctanoic acid is known to induce lipid accumulation in the liver, the impact of perfluorooctanoic acid on different lipid classes has not been fully evaluated. In this study, we performed untargeted lipidomics analysis to investigate the impact of perfluorooctanoic acid on the lipid homeostasis in C57BL/6 male mice. Perfluorooctanoic acid disturbed the lipid profiles in serum and liver, with a variety of lipid classes significantly altered. Greater impacts were observed in the liver lipidome than the serum lipidome. In particular, some lipid clusters in the liver were altered by both high- and low-dose perfluorooctanoic acid exposure, including the increase of unsaturated triglycerides and the decrease of sphingomyelins, saturated phosphatidylcholines, saturated lysophosphatidylcholines, and phospholipid ethers. In parallel with an increase in the liver, a decrease of saturated phosphatidylcholines was found in the serum of high-dose perfluorooctanoic acid-treated mice. The findings from this study are helpful to improve the understanding of perfluorooctanoic acid-induced dysregulation of lipid metabolism and perfluorooctanoic acid-associated health effects in liver.

Docosahexaenoic Acid-Enriched Phosphatidylcholine Exerted Superior Effects to Triglyceride in Ameliorating Obesity-Induced Osteoporosis through Up-Regulating the Wnt/ß-Catenin Pathway.

A growing number of studies reported that obesity is one of the major inducements for osteoporosis by promoting excessive adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Marine-derived DHA-enriched phosphatidylcholine (DHA-PC) exhibited activities to improve ovariectomized-induced osteoporosis and kidney damage. However, the potential effect of DHA-PC and efficacy differences between DHA-PC and traditional DHA (DHA-triglyceride, DHA-TG) on BMSCs differentiation in obesity-induced osteoporosis were not clear. In the present study, obesity-induced osteoporotic mice were supplemented with DHA-TG and DHA-PC for 120 days. Results showed that supplementing with DHA-PC improved the bone mineral density and biomechanical properties, increased the new bone formation rate by 55.2%, and reduced the amount of bone marrow fat to a greater extent than DHA-TG. Further in vitro results showed that DHA-PC significantly promoted the osteogenic differentiation and inhibited the adipogenic differentiation of BMSCs. Mechanistically, DHA-PC supplement up-regulated Wnt/ß-catenin pathway in BMSCs and up-regulated the expression of osteogenic transcription factors, thereby promoting osteogenic differentiation. In summary, DHA-PC exerted a superior effect to DHA-TG in improving obesity-induced osteoporosis. The results provided new evidence for the application of different molecular forms of DHA in treatment of osteoporosis.

Lipid metabolism disorders contribute to hepatotoxicity of ICR mice induced by nitrosamines exposure.

Health risks caused by crucial environmental carcinogens N-nitrosamines triggered ubiquitous attention. As the liver exerted vital function through metabolic process, lipid metabolism disorders have been confirmed as potential drivers for toxicological effects, and the mechanisms of lipid regulation related to hepatotoxicity induced by N-nitrosamines remained largely unclear. In this study, we comprehensively explored the disturbance of hepatic lipid homeostasis in mice induced by nitrosamines. The results implied that nitrosamines exposure induced hepatotoxicity accompanied by liver injury, inflammatory infiltration, and hepatic edema. Lipidomics profiling analysis indicated the decreased levels of phosphatidic acids (PA), phosphatidylcholines (PC), phosphatidylethanolamines (PE), lyso-phosphatidylcholines (LPC), lyso-phosphatidylethanolamines (LPE), diacylglycerols (DAG) and triacylglycerols (TAG), the elevation of ceramides (Cer) and decomposition of free fatty acids (FFA) in high-dose nitrosamines exposure group. Importantly, nitrosamines exposure promoted fatty acid oxidation (FAO) by facilitating fatty acid uptake and decomposition, together with the upregulation of genes associated with FAO accompanied by the activation of inflammatory cytokines TNF-α, IL-1ß and NLRP3. Furthermore, fatty acid translocase CD36-mediated fatty acid oxidation was correlated with the enhancement of oxidative stress in the liver caused by nitrosamines exposure. Overall, our results contributed to the new strategies to interpret the early toxic effects of nitrosamines exposure.

Effect of exogenous lipase on subcutaneous adipose tissue in a porcine animal model.

BACKGROUND: Topical exogenous lipase has been approved for cosmetic use and has been used to mobilize fat from adipocytes. The objective of this study was to determine the effects of exogenous lipase in the subcutaneous adipose tissue. METHODS: Three different concentrations of exogenous lipase 1× (2 Units per ml), 5× (10 units per ml), and 10× (20 units per ml) were applied in a porcine model. Normal saline (NS) solution (as negative control) and phosphatidylcholine (as positive control) were also injected. Skin and subcutaneous tissue biopsies, up to the fascia, were obtained from each injection site on the 3rd day after injection. The number of cells per 20× field was counted as an indirect measurement of the size of the adipocytes. RESULTS: For 1× lipase, the number of cells per field was 47.80 (±7.63) versus 27.26 (±4.93), and 34.66 (±6.84) for NS, and phosphatidylcholine, respectively. For 5× lipase, the count was 36.06 (±4.74) versus 24.13 (±5.18), and 33.2 (±9.34). For 10× lipase, it was 40.06 (±4.35) versus 29.26 (±2.34) and 32.66 (±6.30) (p < .05 for all groups). CONCLUSIONS: A higher number of cells per field were observed in the lipase samples, inferring a decreased volume of adipocytes. No inflammation and/or loss of cell architecture were evidenced in the exogenous lipase groups.

Lipidomic-based investigation into the therapeutic effects of polyene phosphatidylcholine and Babao Dan on rats with non-alcoholic fatty liver disease.

In recent years, with the improvement of people's living standards, non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world. In this paper, the metabolic disorders in Sprague Dawley (SD) rats were induced by a choline-deficient, l-amino acid-defined (CDAA) diet. The therapeutic effects of polyene phosphatidylcholine (PPC) and Babao Dan (BBD) on NAFLD were observed. Lipidomic analysis was performed using ultra-high-performance liquid chromatography-Orbitrap MS, and data analysis and lipid identification were performed using the software LipidSearch. Both PPC and BBD can reduce lipid accumulation in the liver and improve abnormal biochemical indicators in rats, including reduction of triglycerides, total cholesterol, alanine transaminase and aspartate transaminase in serum. In addition, lipids in rat serum were systematically analyzed by lipidomics. The lipidomic results showed that the most obvious lipids with abnormal metabolism in CDAA diet-induced rats were glycerides (triglycerides and diacylglycerols), phospholipids and cholesterol esters. Both BBD and PPC partly reversed the disturbance to lipids induced by the CDAA diet. PPC may be more effective than BBD in alleviating NAFLD because it has a better effect on inhibiting the abnormal accumulation of lipids and reducing the inflammatory reaction in the body.

Efficient Enrichment of Retinal DHA with Dietary Lysophosphatidylcholine-DHA: Potential Application for Retinopathies.

Although decreased retinal docosahexaenoic acid (DHA) is a known risk factor for retinopathy, currently available omega-3 fatty acid supplements, which are absorbed as triacylglycerol (TAG), do not significantly enrich retinal DHA. We tested the hypothesis that lysophospahtidylcholine (LPC)-DHA which is absorbed as phospholipid, would efficiently increase retinal DHA because of the presence of LPC-specific transporter at the blood-retina barrier. In normal rats, LPC-DHA and di-DHA phosphatidylcholine (PC), which generates LPC-DHA during digestion, increased retinal DHA by 101% and 45%, respectively, but TAG-DHA had no significant effect at the same dose (40 mg/kg, 30 days). In normal mice, both sn-1 DHA LPC and sn-2 DHA LPC increased retinal DHA by 80%, but free DHA had no effect. Lipase-treated krill oil (which contains LPC-DHA and LPC-EPA (eicosapentaenoic acid), but not normal krill oil (which has little LPC), increased both retinal DHA (+76%) and EPA (100-fold). Fish oil, however, had no effect, whether lipase-treated or not. These studies show that retinal DHA can be efficiently increased by dietary LPC-DHA, but not by TAG-DHA or free DHA. Since DHA is known to be protective against retinopathy and other eye diseases, this study provides a novel nutraceutical approach for the prevention/treatment of these diseases.

A phospholipid-based formulation for the treatment of airway inflammation in chronic respiratory diseases.

Inflammation, the major hallmark of all chronic respiratory diseases is generally managed by inhaled corticosteroids. However, long term high dose treatment can result in significant side effects. Hence, there is a medical need for non-steroidal anti-inflammatory therapies to address airway inflammation. Phospholipids have been shown to reduce inflammation in several inflammatory conditions; however, their clinical translation has been limited to liposomal formulations traditionally used as drug carriers and their biological activity has not been investigated. Here we report the first application of empty liposomes as an anti-inflammatory treatment in airway inflammation. In the current study, liposomes (UTS-001) were prepared from cholesterol and a synthetic phospholipid (DOPC). The formulation was characterised in terms of size, charge, polydispersity index, morphology and stability as colloidal suspension and freeze-dried nanoparticles. Time-dependant uptake of UTS-001 in airway epithelial cells was observed which was inhibited by nystatin demonstrating that the uptake is via the caveolae pathway. In-vitro, in primary nasal epithelial cells, UTS-001 treatment successfully attenuated IL-6 levels following TNF-α stimulation. Consistent with the in-vitro findings, in-vivo, in the ovalbumin model of allergic airway inflammation, UTS-001 significantly reduced total immune cell counts in bronchoalveolar lavage fluid and reduced airway hyperresponsiveness in response to increasing doses of methacholine challenge. Therefore, our results establish UTS-001 as a potential anti-inflammatory treatment that may be useful as a therapeutic for lung inflammatory diseases.

Prevention of Nonalcoholic Hepatic Steatosis by Shenling Baizhu Powder: Involvement of Adiponectin-Induced Inhibition of Hepatic SREBP-1c.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, and its incidence is increasing annually, but there is currently no specific drug for treating NAFLD. Shenling Baizhu powder (SL) is a safe herbal compound commonly used in clinical practice. Our previous research has shown that SL has the effect of preventing NAFLD, but its specific mechanism has not been determined. In this study, the potential mechanism of SL on NAFLD was explored by in vivo experiments. METHODS: Wistar rats fed a choline-deficient amino acid-defined diet (CDAA) were treated with SL for 8 weeks. Then, serum samples were collected to obtain biochemical indicators; adipose tissue and liver samples were collected for pathological detection; a moorFLPI-2 blood flow imager was used to measure liver microcirculation blood flow, and a rat cytokine array was used to screen potential target proteins. The expression of liver adiponectin/SREBP-1c pathway-related proteins was determined by Western blotting. RESULTS: SL effectively reduced the liver wet weight, as well as the levels of total cholesterol (TC) and triglyceride (TG) in the liver, and ameliorated liver injury in CDAA-fed rats. Pathological examinations showed that SL markedly reduced liver lipid droplets and improved liver lipid accumulation. In addition, the detection of liver blood flow showed that SL increased liver microcirculation in CDAA-fed rats. Through the cytokine array, a differentially expressed cytokine, namely, adiponectin, was screened in the liver. Western blotting assays showed that SL increased the expression of adiponectin and phosphoacetyl-CoA Carboxylase (p-ACC) in the liver and decreased the expression of steroid regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS). CONCLUSION: These results suggest that SL can increase the levels of adiponectin in the liver and serum and can inhibit the expression of SREBP-1c, thereby regulating systemic lipid metabolism and reducing liver lipid accumulation.

Recovery of brain DHA-containing phosphatidylserine and ethanolamine plasmalogen after dietary DHA-enriched phosphatidylcholine and phosphatidylserine in SAMP8 mice fed with high-fat diet.

BACKGROUND: Glycerophospholipids were the main components of cerebral cortex lipids, and there was a close association between lipid homeostasis and human health. It has been reported that dietary DHA-enriched phosphatidylcholine (DHA-PC) and phosphatidylserine (DHA-PS) could improve brain function. However, it was unclear that whether supplementation of DHA-PC and DHA-PS could change lipid profiles in the brain of dementia animals. METHODS: SAMP8 mice was fed with different diet patterns for 2 months, including high-fat diet and low-fat diet. After intervention with DHA-PC and DHA-PS for another 2 months, the lipid profile in cerebral cortex was determined by lipidomics in dementia mice. RESULTS: High-fat diet could significantly decrease the levels of DHA-containing PS/pPE, DPA-containing PS, and AA-containing PE, which might exhibit the potential of lipid biomarkers for the prevention and diagnosis of AD. Notably, DHA-PC and DHA-PS remarkably recovered the lipid homeostasis in dementia mice. These might provide a potential novel therapy strategy and direction of dietary intervention for patients with cognitive decline. CONCLUSIONS: DHA-PC and DHA-PS could recover the content of brain DHA-containing PS and pPE in SAMP8 mice fed with high-fat diet.

Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity in Caenorhabditis elegans.

Phosphatidylcholine is one of the major phospholipids comprising cellular membrane and is known to have several health-promoting activities, including the improvement of brain function and liver repair. In this paper, we examine the in vivo effect of dietary supplementation with phosphatidylcholine on the response to environmental stressors and aging in C. elegans. Treatment with phosphatidylcholine significantly increased the survival of worms under oxidative stress conditions. However, there was no significant difference in response to stresses caused by heat shock or ultraviolet irradiation. Oxidative stress is believed to be one of the major causal factors of aging. Then, we examined the effect of phosphatidylcholine on lifespan and age-related physiological changes. Phosphatidylcholine showed a lifespan-extending effect and a reduction in fertility, possibly as a tradeoff for long lifespan. Age-related decline of motility was also significantly delayed by supplementation with phosphatidylcholine. Interestingly, the expressions of well-known longevity-assuring genes, hsp-16.2 and sod-3, were significantly upregulated by dietary intervention with phosphatidylcholine. DAF-16, a transcription factor modulating stress response genes, was accumulated in the nucleus by phosphatidylcholine treatment. Increase of the ROS level with phosphatidylcholine suggests that the antioxidant and lifespan-extending effects are due to the hormetic effect of phosphatidylcholine. Phosphatidylcholine also showed a protective effect against amyloid beta-induced toxicity in Alzheimer's disease model animals. Experiments with long-lived mutants revealed that the lifespan-extending effect of phosphatidylcholine specifically overlapped with that of reduced insulin/IGF-1-like signaling and required DAF-16. These findings showed the antioxidant and antiaging activities of phosphatidylcholine for the first time in vivo. Further studies focusing on the identification of underlying cellular mechanisms involved in the antiaging effect will increase the possibility of using phosphatidylcholine for the development of antiaging therapeutics.

DHA-PC protects kidneys against cisplatin-induced toxicity and its underlying mechanisms in mice.

Cisplatin is an effective chemotherapeutic agent used in the treatment of various cancers. However, its use is usually complicated by nephrotoxic side effects, which limit its clinical application. Interestingly, DHA supplementation has been found to exhibit anticancer activity without any side effects. It is noted that DHA-PC has been applied in the treatment of kidney diseases. Our aim in the current study was to investigate whether DHA-PC treatment could alleviate cisplatin-induced nephrotoxicity using a Balb/c mice model. Our results showed that DHA-PC could significantly prolong the survival time, while the traditional DHA had no remarkable changes. In addition, short supplements of DHA-PC alleviated the cisplatin-induced kidney dysfunction, such as increased levels of blood urea nitrogen and creatinine. DHA-PC could protect the kidneys against cisplatin-induced toxicity, which might be attributed to the sirtuin 1 activation and the inhibition of oxidative stress and apoptosis. These findings suggest that DHA-PC might be a new dietary strategy for the treatment of nephrotoxicity.

Incorporation of Baccharis dracunculifolia DC (Asteraceae) leaf extract into phosphatidylcholine-cholesterol liposomes improves its anti-inflammatory effect in vivo.

The aerial parts of Baccharis dracunculifolia (BdE) is used in the Brazilian folk medicine to treat inflammatory conditions. Here we examined the ability of free and liposomal BdE to modulate reactive oxygen species generation in human neutrophils in vitro and zymosan-induced acute joint inflammation in Wistar rats. We prepared biocompatible liposomes of soya phosphatidylcholine and cholesterol with low diameter, homogeneous size distribution, and neutral surface charge. Free BdE decreased joint swelling, total leucocyte and neutrophil infiltration, and the synovial levels of tumour necrosis factor-α and interleukins 6 and 1ß. Incorporation of BdE into liposomes preserved its capacity to inhibit the neutrophil superoxide anion and total reactive oxygen species generation, and improved its anti-inflammatory effect in vivo by decreasing the effective BdE dose by nearly sixfold. The same liposome type lowered the effective dose of caffeic acid by nearly sixteenfold. Therefore, incorporation of BdE into phosphatidylcholine-cholesterol liposomes improves its anti-inflammatory effect.

Phosphatidylcholine could protect the defect of zearalenone exposure on follicular development and oocyte maturation.

Zearalenone (ZEA) is a well-known exogenous endocrine disruptor and can lead to severe negative effects on the human and animal reproductive process. Using a follicle culture model, we have previously shown that ZEA exposure significantly affected the follicular development and antrum formation but the underlying mechanisms are not well known. Therefore, in this study, we explored the metabolomic changes of granulosa cell (GC) culture media with or without ZEA exposure. The results showed that ZEA significantly increased phosphatidylcholine or phosphatidyl ethanolamine adducts in culture medium. A comprehensive analysis with the metabolome data from follicular fluid of small and large antral follicles showed that lyso phosphatidylcholine (LPC) was accumulated during follicle growth, but was depleted by ZEA exposure. Exogenous supplement with LPC to the follicle growth media or oocyte maturation media can partly protect the defect of ZEA exposure on follicular antrum formation and oocyte maturation. Taken together, our results demonstrate that ZEA exposure hinders the follicular growth and exogenous LPC can practically protect the defect of ZEA on follicular development and oocyte maturation.

Pectin influences the kinetics of in vitro lipid digestion in oil-in-water emulsions.

Oil-in-water emulsions were prepared with 5% (w/v) carrot-enriched olive oil and stabilized with Tween 80 (TW), phosphatidylcholine (PC), citrus pectin (CP) or a combination of these emulsifiers. Additionally, the methylesterification degree (DM) of citrus pectin was modified, resulting in three different studied pectin structures: CP82, CP38 and CP10. All initial emulsions presented small initial oil droplet sizes and were submitted to an in vitro simulated gastric and small intestinal phase. The latter was executed in a kinetic way to determine the time dependency of the lipolysis reaction, micelle formation and carotenoid bioaccessibility. The results showed that the pectin DM mainly influenced the reaction rate constants, while the emulsifier (combination) determined the extent of lipolysis and carotenoid bioaccessibility. Moreover, a direct relation was observed between the lipolysis reaction and bioaccessibility extent. The presented study showed that targeted emulsion design can be used to tailor lipid digestion kinetics.

Specific Phospholipids Regulate the Acquisition of Neuronal and Astroglial Identities in Post-Mitotic Cells.

Hitherto, the known mechanisms underpinning cell-fate specification act on neural progenitors, affecting their commitment to generate neuron or glial cells. Here, we show that particular phospholipids supplemented in the culture media modify the commitment of post-mitotic neural cells in vitro. Phosphatidylcholine (PtdCho)-enriched media enhances neuronal differentiation at the expense of astroglial and unspecified cells. Conversely, phosphatidylethanolamine (PtdEtn) enhances astroglial differentiation and accelerates astrocyte maturation. The ability of phospholipids to modify the fate of post-mitotic cells depends on its presence during a narrow time-window during cell differentiation and it is mediated by the selective activation of particular signaling pathways. While PtdCho-mediated effect on neuronal differentiation depends on cAMP-dependent kinase (PKA)/calcium responsive element binding protein (CREB), PtdEtn stimulates astrogliogenesis through the activation of the MEK/ERK signaling pathway. Collectively, our results provide an additional degree of plasticity in neural cell specification and further support the notion that cell differentiation is a reversible phenomenon. They also contribute to our understanding of neuronal and glial lineage specification in the central nervous system, opening up new avenues to retrieve neurogenic capacity in the brain.

Inflammatory pain control by blocking oxidized phospholipid-mediated TRP channel activation.

Phospholipids occurring in cell membranes and lipoproteins are converted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque formation. Here, OxPL were characterized as novel targets in acute and chronic inflammatory pain. Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and its derivatives were identified in inflamed tissue by mass spectrometry and binding assays. They elicited calcium influx, hyperalgesia and induced pro-nociceptive peptide release. Genetic, pharmacological and mass spectrometric evidence in vivo as well as in vitro confirmed the role of transient receptor potential channels (TRPA1 and TRPV1) as OxPAPC targets. Treatment with the monoclonal antibody E06 or with apolipoprotein A-I mimetic peptide D-4F, capturing OxPAPC in atherosclerosis, prevented inflammatory hyperalgesia, and in vitro TRPA1 activation. Administration of D-4F or E06 to rats profoundly ameliorated mechanical hyperalgesia and inflammation in collagen-induced arthritis. These data reveal a clinically relevant role for OxPAPC in inflammation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC.

Selective effect of phosphatidylcholine on the lysis of adipocytes.

Obesity, a serious health risk factor, is often associated with depression and negatively affects many aspects of life. Injection of a formula comprising phosphatidylcholine (PPC) and deoxycholate (DC) has emerged as an alternative to liposuction in the reduction of local fat deposits. However, the formula component mainly responsible for this effect and the mechanism behind the actions of the components with respect to fat reduction are unknown. Here, we investigate the specific effects of PPC and DC on adipocyte viability. When exposed to PPC or DC, 3T3L1 preadipocytes and differentiated adipocytes showed dose dependent decrease in cell viability. Interestingly, while DC mediated cell death was non-specific to both preadipocytes and adipocytes, PPC specifically induced a decrease in mature adipocyte viability, but had less effect on preadipocytes. Injection of PPC and DC into inguinal fat pads caused reduction in size. PPC injections preferentially decreased gene expression in mature adipocytes, while a strong inflammatory response was elicited by DC injection. In line with the decreased adipocyte viability, exposure of differentiated adipocytes to PPC resulted in triglyceride release, with a minimal effect on free fatty acids release, suggesting that its fat-reducing effect mediated mainly through the induction of adipocyte cell death rather than lipolysis. Taken together, it appears that PPC specifically affects adipocytes, and has less effect on preadipocyte viability. It can therefore be a promising agent to selectively reduce adipose tissue mass.

Effect of soybean phosphatidylcholine on lipid profile of bovine oocytes matured in vitro.

The phospholipid (PL) composition of embryo and oocyte membranes affects thermal phase behavior and several physicochemical properties such as fluidity and permeability. The characterization of PL profiles and the development of suitable in vitro maturation (IVM) protocols, that are able to modify membrane's composition, may result in significant improvements in oocyte developmental potential and cryotolerance. Using soybean phosphatidylcholine (PC) as a model supplement, we evaluated the effect of PL supplementation during IVM on bovine cumulus-oocyte-complex (COC). Substantial changes in the lipid profiles of oocyte membrane were observed and associated with pre-implantation data. The propensity of the PC supplement to become soluble in the maturation medium and/or diffuse into mineral oil was also assessed. Oocytes were matured in TCM without supplementation, i.e. control, (n=922) or supplemented with 50 or 100µM PC (n=994). The maturation media and mineral oil pre- and post- IVM, along with control and PC-treated oocytes were then analyzed using matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS), and the lipid profiles were compared via principal component analysis (PCA). Soybean PCs are bioavailable and stable in IVM medium; further, PCs did not diffuse to the mineral oil, which also remained unaltered by the metabolism of treated oocytes. PC supplementation at 100µM resulted in substantially greater relative abundances of polyunsatured PL, namely PC (32:1), PC (34:2), PC (36:6), PC (36:4), and PC (38:6), in oocyte membrane. These differences indicated that short-term exposure to the PC supplement could indeed modify the lipid composition of IVM-oocytes in a dose-dependent manner. Membrane incorporation of polyunsaturated molecular species of PC was favored, and does so without compromising the viability of the subsequent embryo in regards to cleavage, blastocyst development and hatching rate. The reported approach will allow for the development of novel strategies to modulate oocyte membrane dynamics and structure.

MALDI-TOF/TOF Mass Spectrometric Determination and Antioxidative Activity of Purified Phosphatidylcholine Fractions from Shrimp Species.

Purification, characterization, and antioxidative activity in vitro of shrimp phosphatidylcholines (PCs) were investigated. The molecular structures of shrimp PCs were determined by MALDI-TOF/TOF MS. The MS2 fragments produced from protonated PC precursors and sodiated PC precursors were identified. The specific fragments including [M + Na - trimethylamine]+, [M + Na - 205]+, [M + Na - RCOOH - trimethylamine]+, and [M + H - RCOOH - trimethylamine]+ could distinguish the precursor type to confirm PC molecular structures. The antioxidative activities of purified shrimp PC fractions were evaluated by assay of DPPH free radical scavenging activity, and their effects on the oxidative stability of camellia oil were measured by monitoring changes in the peroxide value assay during oxidation. The PC fractions from Penaeus chinesis and Macrobranchium nipponense showed stronger antioxidative activities than those of other species. All of the shrimp PCs at 0.2% (w/w) improved the oxidative stability of camellia oil significantly (P < 0.05) compared to controls. The experimental findings suggest that shrimp PCs might be a valuable source of natural antioxidants for edible oils or other food dispersions.

Twisting of the spermatic cord: ischemia and reperfusion, toxicogenetic evaluation, and the effects of phosphatidylcholine in pre-clinical trials.

Phosphatidylcholine is the main phospholipid present in cell membranes and in lipoproteins, and can interfere with various biological processes. This lipid also has antioxidant activity, and protects against damage caused by free radicals under conditions of ischemia/reperfusion. Therefore, the present study was designed to evaluate toxicogenetic damage caused by twisting of the spermatic cord in ischemia/reperfusion, and whether phosphatidylcholine plays a role in conditions of ischemia/reperfusion in preclinical trials. The results indicate that spermatic cord torsion does not cause genotoxic damage or mutagenesis. A dose of 300 mg/kg of phosphatidylcholine is toxic and is thus not recommended. However, a dose of 150 mg/kg does not promote toxicogenetic damage, and though it does not statistically prevent tissue damage occurring from lack of oxygenation and nutrition of testicular cells, it has a tendency to reduce this damage. Therefore, this research suggests that further studies should be conducted to clarify this tendency and to provide a better explanation of the possible therapeutic effects of phosphatidylcholine in cytoprotection of germ cells affected by ischemia/reperfusion.