A Review of Biopolymers’ Utility as Emulsion Stabilizers

Polysaccharides, polynucleotides, and polypeptides are basic natural polymers. They have various applications based on their properties. This review mostly discusses the application of natural polymers as emulsion stabilizers. Natural emulsion stabilizers are polymers of amino acid, nucleic acid, carbohydrate, etc., which are derived from microorganisms, bacteria, and other organic materials. Plant and animal proteins are basic sources of natural emulsion stabilizers. Pea protein-maltodextrin and lentil protein feature entrapment capacity up to 88%, (1–10% concentrated), zein proteins feature 74–89% entrapment efficiency, soy proteins in various concentrations increase dissolution, retention, and stability to the emulsion and whey proteins, egg proteins, and proteins from all other animals are applicable in membrane formation and encapsulation to stabilize emulsion/nanoemulsion. In pharmaceutical industries, phospholipids, phosphatidyl choline (PC), phosphatidyl ethanol-amine (PE), and phosphatidyl glycerol (PG)-based stabilizers are very effective as emulsion stabilizers. Lecithin (a combination of phospholipids) is used in the cosmetics and food industries. Various factors such as temperature, pH, droplets size, etc. destabilize the emulsion. Therefore, the emulsion stabilizers are used to stabilize, preserve and safely deliver the formulated drugs, also as a preservative in food and stabilizer in cosmetic products. Natural emulsion stabilizers offer great advantages because they are naturally degradable, ecologically effective, non-toxic, easily available in nature, non-carcinogenic, and not harmful to health.

Role of Autophagy in Phosphatidyl- Glycerol Facilitated Cholesterol Clearance from the Endolysosomal System of Npc-1 Deficient Cells

Niemann Pick Type C (NPC) Disease is a rare lysosomal storage disorder in which one of the genes that codes for either the NPC-1 or NPC-2 pro-tein is mutated, causing cell lysosomes to accumu-late cholesterol and lipids. Previous studies discov-ered that a unique late endosomal/lysosomal phos-pholipid, lysobisphosphatidic acid (LPBA), is in-volved in cholesterol clearance from late endo-somes. It has also been shown that exogenous treat-ment of the NPC-1 deficient cells with LBPA’s precur-sor, phosphatidylglycerol (PG), leads to LBPA enrich-ment and subsequent endolysosomal cholesterol clearance. Autophagy is a mechanism of cellular clearance in the endolysomal system and we are in-terested to see if it is a partial route in cholesterol clearance during PG treatment of NPC-1 deficient cells. To do so, we silenced the gene that codes for an essential protein in the autophagy pathway, mak-ing the cells autophagy deficient. We then treated the cells with PG, measured the amount of choles-terol clearance in those cells, and compared it to cells with normal autophagy. We found significantly less cholesterol clearance by PG in cells with defec-tive autophagy, confirming that autophagy is in-volved as a partial route in cholesterol clearance dur-ing PG treatment, but not enough of a difference to conclude that it is a major underlying mechanism.

Lipidomic profiling of the developing kernel clarifies the lipid metabolism of Paeonia ostii

Lipid components in the developing kernel of Paeonia ostii were determined, and the fatty acid (FA) distributions in triacylglycerol and phospholipids were characterized. The lipids in the kernel were mainly phospholipids (43%), neutral glycerides (24%), fatty acyls (26%), and sphingolipids (4.5%). The dominant neutral glycerides were TAG and diacylglycerol. The PL components included phosphatidic acid, phosphatidyl glycerol, phosphatidyl choline, phosphatidyl serine, phosphatidyl inositol, and phosphatidyl ethanolamine. As the kernel developed, the profiles of the molecular species comprising TAG and PL changed, especially during the earlier phases of oil accumulation. During rapid oil accumulation, the abundances of sphingosine-1-phosphate, pyruvic acid, stearic acid, and alpha-linolenic acid changed significantly; the sphingolipid metabolism and unsaturated FAs biosynthesis pathways were significantly enriched in these differentially abundant metabolites. Our results improve our understanding of lipid accumulation in tree peony seeds, and provide a framework for the analysis of lipid metabolisms in other oil crops.

Changes of Neuropathy Target Esterase Affect Phospholipid Homeostasis in SK-N-SH Cells

Neuropathy target esterase (NTE), is a membrane protein located in the endoplasmic reticulum (ER). NTE has the activity of phospholipase B and can catalyze the deacylation of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) to glycerylcholine (GPC). It is phosphorylated and aged by organophosphorus compounds (OPs), that induce delayed neuropathy in humans and sensitive animals. Our previous study has reported that the disruption of ER phospholipid homeostasis caused by the NTE inhibition may contribute to the initiation of the organophosphate-induced delayed neurotoxicity (OPIDN), while it is unknown how the disturbed phospholipid homeostasis initiates OPIDN. It is difficult to change phospholipids in in vivo experiments. Therefore, an in vitro model is urgently needed to explain the role of phospholipid homeostasis disorders in OPIDN. In this study, we altered the expression of NTE in SK-N-SH cells and determined its phospholipid component by using HPLC-MS. Our results showed that the changes of NTE affected the levels of PC, sphingomyelin (SM), phosphatidylethanolamine (PE), phosphatidylserine (PS), lysophosphatidylserine (LPS), phosphatidyl-glycerol (PG), and phosphatidylinositol (PI). Our results were consistent with the in vivo results. Furthermore, our findings indicate that the SK-N-SH cell model is a significantly useful method for the further research on how the changes of phospholipid homeostasis initiate the OPIDN, which is easier than the in vivo experiments in practice.

Modified Bacterial Lipids Which Alter Membrane Surface Charge Reduce Binding of Antimicrobial Peptides

ABSTRACTAntimicrobial peptides (AMPs) initiate killing of bacteria by binding to and destabilizing their membranes. The multiple peptide resistance factor (MprF) provides a defence mechanism for bacteria against a broad range of AMPs. MprF reduces the negative charge of both Gram-positive and Gram--negative bacterial membranes through enzymatic conversion of the anionic lipid phosphatidyl glycerol (PG) to either zwitterionic alanyl-phosphatidyl glycerol (Ala-PG) or cationic lysylphosphatidyl glycerol (Lys-PG). The resulting change in membrane charge is suggested to reduce AMP-membrane binding and hinder downstream AMP activity. Using molecular dynamics to investigate the effects of these modified lipids on AMP-binding to model membranes, we show that AMPs have substantially reduced affinity for model membranes containing Ala-PG or Lys-PG. A total of ~7000 simulations are used to define the relationship between bilayer composition and binding for 5 different membrane active peptides. The reduction of degree of interaction of a peptide with the membrane is shown to correlate with the change in membrane surface charge density. Free energy profile (potential of mean force) calculations reveal that these lipid modifications alter the energy barrier to peptide helix penetration of the bilayer. These results will enable us to guide design of novel peptides which address the issue of resistance via MprF-mediated membrane modification.

Cardiolipin is an Optimal Phospholipid for the Assembly, Stability, and Proper Functionality of the Dimeric Form of NhaA Na+/H+ Antiporter

Cardiolipin (CL) was shown to bound to the dimer interface of NhaA Na+/H+ antiporter. Here, we explore the cardiolipin-NhaA interaction both in vitro and in vivo. Using a novel and straightforward in-vitro assay in which n-dodecyl β-D maltoside (DDM) detergent is used to delipidate the dimer interface and to split the dimers into monomers; the monomers are subsequently exposed to cardiolipin or the other E. coli phospholipids. Most efficient reconstitution of dimers is observed by cardiolipin. This assay is likely to be applicable to future studies of protein–lipid interactions. In-vivo experiments further reveal that cardiolipin is necessary for NhaA survival. Although less efficient phosphatidyl-glycerol (PG) can also reconstitute NhaA monomers to dimers. We also identify a putative cardiolipin binding site. Our observations may contribute to drug design, as human NhaA homologues, which are involved in severe pathologies, might also require specific phospholipids.