Use of high-intensity ultrasound as a pre-treatment for complex coacervation from whey protein isolate and iota-carrageenan.

The aim of this work was to evaluate the influence of high intensity ultrasound (HIUS) treatment on the molecular conformation of whey protein isolated (WPI) as a previous step for complex coacervation with iota carrageenan (IC) and its effect on the surface functional properties of complex coacervates (CC). Both biopolymers were hydrated (1% w/w) separately. A WPI suspension was treated with an ultrasonic bath (40 kHz, 600 W, 30 and 60 min, 100% amplitude). A non-sonicated protein was used as a control. Coacervation was achieved by mixing WPI and IC dispersions (10 min). FTIR-ATR analysis (400-4000 cm-1) detected changes after sonication on WPI secondary structure (1600-1700 cm-1), electrostatic interaction between WPI and IC by electronegative IC charged groups like sulfate (1200-1260 cm-1), anhydrous oxygen of the 3.6 anhydro-D-galactose (940-1066 cm-1) and the electropositive regions of WPI. Rheology results showed pseudoplastic behavior of both IC and WPI-IC with a significant change in viscosity level. Further, HIUS treatment had a positive effect on the emulsifying properties of the WPI-IC coacervates, increasing the time foaming (30 min) and emulsion stability (1 month) percentage. HIUS and complex coacervation proved to be an efficient tool to improve the surface functional properties of WPI.

High-intensity ultrasound pretreatment influence on whey protein isolate and its use on complex coacervation with kappa carrageenan: Evaluation of selected functional properties.

The aim of this work was to evaluate the influence of high-intensity ultrasound (HIUS) treatment on whey protein isolate (WPI) molecular structure as a previous step for complex coacervation (CC) with kappa-carrageenan (KC) and its influence on CC functional properties. Protein suspension of WPI (1% w/w) was treated with an ultrasound probe (24 kHz, 2 and 4 min, at 50 and 100% amplitude), non HIUS pretreated WPI was used as a control. Coacervation was achieved by mixing WPI and KC dispersions (10 min). Time and amplitude of the sonication treatment had a direct effect on the molecular structure of the protein, FTIR-ATR analysis detected changes on pretreated WPI secondary structure (1600-1700 cm-1) after sonication. CC electrostatic interactions were detected between WPI positive regions, KC sulfate group (1200-1260 cm-1), and the anhydrous oxygen of the 3,6 anhydro-D-galactose (940-1066 cm-1) with a partial negative charge. After ultrasound treatment, a progressive decrease in WPI particle size (nm) was detected. Rheology results showed pseudoplastic behavior for both, KC and CC, with a significant change on the viscosity level. Further, volume increment, stability, and expansion percentages of CC foams were improved using WPI sonicated. Besides, HIUS treatment had a positive effect on the emulsifying properties of the CC, increasing the time emulsion stability percentage. HIUS proved to be an efficient tool to improve functional properties in WPI-KC CC.

Natural mechanisms and artificial PEG-induced mechanism that repair traumatic damage to the plasmalemma in eukaryotes.

Eukaryotic tissues are composed of individual cells surrounded by a plasmalemma that consists of a phospholipid bilayer with hydrophobic heads that bind cell water. Bound-water creates a thermodynamic barrier that impedes the fusion of a plasmalemma with other membrane-bound intracellular structures or with the plasmalemma of adjacent cells. Plasmalemmal damage consisting of small or large holes or complete transections of a cell or axon results in calcium influx at the lesion site. Calcium activates fusogenic pathways that have been phylogenetically conserved and that lower thermodynamic barriers for fusion of membrane-bound structures. Calcium influx also activates phylogenetically conserved sealing mechanisms that mobilize the gradual accumulation and fusion of vesicles/membrane-bound structures that seal the damaged membrane. These naturally occurring sealing mechanisms for different cells vary based on the type of lesion, the type of cell, the proximity of intracellular membranous structures to the lesion and the relation to adjacent cells. The reliability of different measures to assess plasmalemmal sealing need be carefully considered for each cell type. Polyethylene glycol (PEG) bypasses calcium and naturally occurring fusogenic pathways to artificially fuse adjacent cells (PEG-fusion) or artificially seal transected axons (PEG-sealing). PEG-fusion techniques can also be used to rapidly rejoin the closely apposed, open ends of severed axons. PEG-fused axons do not (Wallerian) degenerate and PEG-fused nerve allografts are not immune-rejected, and enable behavioral recoveries not observed for any other clinical treatment. A better understanding of natural and artificial mechanisms that induce membrane fusion should provide better clinical treatment for many disorders involving plasmalemmal damage.