Lipid crystallinity of oil-in-water emulsions alters in vitro.

10 wt% oil-in-water emulsions with varied palm olein and stearin PO:PS ratios stabilized with 0.8 wt% Tween80 and tempered to obtain partially crystalline (CR) droplets (cooled from 80 to 4 °C and held overnight to induce nucleation/crystallization) or undercooled liquid (UC) droplets (cooled from 80 °C to 37 °C) produced emulsions with constant droplet size and polymorphism. However, zeta-potential decreased in undercooled emulsions due to crystallization/orientation of interfacial Tween, increasing alignment and ultimately a greater dipole moment. Significant differences in overall bioaccessibility between PO and PS present for the CR (PO bioaccessible fraction was 91%, whereas PS was 60%) and UC emulsions (PO and PS bioaccessibility were 96% and 77%).When only the solid fat content differs, and all other physical attributes remain constant, lipid digestibility decreases with increasing solid fat content; these findings, along with others, can be employed during food formulation and design more healthful foods.

A comprehensive perspective of food nanomaterials.

Nanotechnology is a rapidly developing toolbox that provides solutions to numerous challenges in the food industry and meet public demands for healthier and safer food products. The diversity of nanostructures and their vast, tunable functionality drives their inclusion in food products and packaging materials to improve their nutritional quality through bioactive fortification and probiotics encapsulation, enhance their safety due to their antimicrobial and sensing capabilities and confer novel sensorial properties. In this food nanotechnology state-of-the-art communication, matrix materials with particular focus on food-grade components, existing and novel production techniques, and current and potential applications in the fields of food quality, safety and preservation, nutrient bioaccessibility and digestibility will be detailed. Additionally, a thorough analysis of potential strategies to assess the safety of these novel nanostructures is presented.

Water immobilization by glass microspheres affects biological activity.

We recently reported that the water holding capacity of myofibrillar protein hydrogels could be increased upon addition of small amounts of microparticles, particularly glass microspheres. Glass microspheres were found to decrease the spin-spin relaxation time (T2) of water protons in the gels, which was interpreted as enhanced water binding by the glass. We were thus interested in determining whether the observed effects on water proton relaxation were a direct consequence of water-glass interactions. Here we show how glass microspheres reduce the mobility of pure water, reflected in large decreases in the T2 of water protons, decreases in the self-diffusion coefficient of water molecules, a lower water activity, and strengthening of O-H bonds. Even though glass is considered an inert material, glass microspheres were shown to inhibit the growth of human embryonic kidney cells, and stimulate or inhibit the growth of leukemia and monocytic lymphoma cells in vitro, depending on dose and time. The germination of alfalfa seeds and the growth of E.coli cells were also inhibited upon exposure to glass microspheres. This work indicates that the properties and behavior of materials, even ones considered inert, can be affected by their size. These observations suggest possible toxicological consequences of exposure to microparticles, but also open us possibilities to affect cellular/organism function via modulation of macromolecular hydration.

Inhibition of intracellular dipeptidyl peptidases 8 and 9 enhances parthenolide's anti-leukemic activity.

Parthenolide is selectively toxic to leukemia cells; however, it also activates cell protective responses that may limit its clinical application. Therefore, we sought to identify agents that synergistically enhance parthenolide's cytotoxicity. Using a high-throughput combination drug screen, we identified the anti-hyperglycemic, vildagliptin, which synergized with parthenolide to induce death of the leukemia stem cell line, TEX (combination index (CI)=0.36 and 0.16, at effective concentration (EC) 50 and 80, respectively; where CI <1 denotes statistical synergy). The combination of parthenolide and vildagliptin reduced the viability and clonogenic growth of cells from acute myeloid leukemia patients and had limited effects on the viability of normal human peripheral blood stem cells. The basis for synergy was independent of vildagliptin's primary action as an inhibitor of dipeptidyl peptidase (DPP) IV. Rather, using chemical and genetic approaches we demonstrated that the synergy was due to inhibition of the related enzymes DPP8 and DPP9. In summary, these results highlight DPP8 and DPP9 inhibition as a novel chemosensitizing strategy in leukemia cells. Moreover, these results suggest that the combination of vildagliptin and parthenolide could be useful for the treatment of leukemia.

Effect of dextran sulfate sodium and acute exercise on mouse intestinal inflammation and lymphocyte cytochrome c levels.

AIM: Athletes may experience gastrointestinal disturbances during intense exercise. Using a mouse model, we determined the influence of acute exercise (AE) and dextran sulfate sodium (DSS), a chemical known to induce intestinal inflammation, on: 1) inflammatory changes within small and large intestine, 2) extent of cell death as measured by cytochrome c levels in intestinal lymphocytes (IL) and 3) the effects of bovine lactoferrin (bLf), a dietary protein with anti-inflammatory properties, on these parameters. METHODS: DSS was given as 5% w/v in water for 4 days. AE consisted of 3 bouts of 90 min of exhaustive treadmill exercise, each separated by 24 h, with sacrifice before, immediately after, or 24 h after the final exercise bout. Mice were fed 2% bLf or control diet for 2 weeks before AE or DSS. Tissue inflammation was determined by histology and IL cytochrome c levels by Western blotting. RESULTS: AE increased plasma 8-iso-PGF2a, a marker of oxidative stress, immediately after relative to before exercise (P<0.01). Cytochrome c levels were elevated following bLf (P<0.01) and DSS (P<0.05) treatment whereas AE had no significant effect. DSS, but not AE, produced histological changes suggestive of intestinal inflammation with no attenuation by bLf. CONCLUSIONS: Three bouts of AE were not associated with intestinal inflammation or IL death in this animal model. Gastrointestinal disturbances arising from intense exercise in humans may not be due to direct inflammatory damage although this remains to be determined clinically.

Repeated exercise in mice alters expression of IL-10 and TNF-alpha in intestinal lymphocytes.

Intestinal inflammation is characterized by mucosal damage that may arise, in part, to imbalances in pro- and anti-inflammatory cytokines. The purpose of this study was to describe the effects of repeated bouts of strenuous exercise on cytokine expression in mouse intestinal lymphocytes (IL). Thirty-four female C57BL/6 mice were randomly assigned to three groups: three repeated bouts of treadmill running separated by 24h followed by sacrifice immediately or after a 24h period or a sedentary (no exercise) control. The pro-inflammatory cytokine, TNF-alpha, and the anti-inflammatory cytokine, IL-10, were measured in IL by Western blotting. IL-10 concentration increased by 48% (p<0.05) in the immediate group compared to the sedentary control. TNF-alpha levels in mouse IL were significantly lower 24h after completion of the exercise protocol compared to the immediate group (p<0.05). The results suggest a possible physiological compensation in which intestinal lymphocytes increase the expression of IL-10 in response to exercise-induced stress.

Effect of repeated exercise stress on caspase 3, Bcl-2, HSP 70 and CuZn-SOD protein expression in mouse intestinal lymphocytes.

The purpose of this study was to characterize the expression of apoptosis (caspase 3, Bcl-2) and survival (HSP 70, antioxidant CuZn-SOD) proteins in intestinal lymphocytes (IL) of mice after repeated exercise stress. Plasma corticosterone concentration was greater than twofold higher immediately after exercise compared with the non-exercised condition. IL numbers decreased 24 h after cessation of exercise (p<0.05); this was associated with increased caspase 3 (p<0.05), HSP 70 (p<0.001) and CuZn-SOD (p<0.05) expression in IL immediately after exercise relative to IL from non-exercised mice. Expression of these proteins returned to control levels 24 h after the cessation of exercise stress.

Freewheel exercise training modifies pro- and anti-apoptotic protein expression in mouse splenic lymphocytes.

The purpose of this study was to examine the effect of voluntary training in mice on the expression of apoptotic proteins in splenic lymphocytes following acute exercise. Thirty-three mice were randomized to four treatments: 1) control group (no training and no acute exercise), 2) training, no acute exercise, 3) no training, acute exercise and 4) training, acute exercise. Mice were sacrificed immediately after acute exercise. Western immunoblotting was used to detect apoptosis in splenic lymphocytes for concentrations of anti- (Bcl-2) and pro-apoptotic (caspase 3) proteins. Plasma corticosterone was used as an index of exercise stress. Trained mice not given acute exercise challenge had elevated Bcl-2 (p < 0.05) and lower caspase 3 (p < 0.05) levels relative to control mice. Following the acute exercise challenge, however, trained and untrained mice did not differ in the concentrations of these proteins in splenocytes. Thus, freewheel exercise training in mice reduces splenic lymphocyte apoptosis when tissue samples are obtained at rest but not after acute exercise.