Chocolate swelling during storage caused by fat or moisture migration.

Quantification of swelling in dark chocolate subjected to fat or moisture migration was conducted using a new method based on confocal chromatic displacement sensor. The nondestructive method allowed for the height profile of dark chocolate samples to be scanned with a sensitivity of ± 2.8 µm. By performing multiple scans on each sample prior to and after being subjected to fat or moisture migration, the induced swelling could be quantified. Applying the new method on confectionery systems revealed that fat and moisture migration generate different swelling behavior/kinetics in dark chocolate during storage. Moisture migration resulted in a rapid swelling once a water activity of 0.8 was reached in the chocolate, probably by interaction and absorption of moisture by the particulate solids. Fat migration also affected the swelling behavior in chocolate, possibly by inducing phase transitions in the continuous cocoa butter phase. Migrating fat also proved to induce a more pronounced swelling than the same amount of absorbed moisture which further consolidated that the observed swelling caused by fat or moisture migration is a result of significant different mechanisms.

A critical review of the quality and safety of BADGE-based epoxy coatings for cans: implications for legislation on epoxy coatings for food contact.

BADGE-based epoxy resins have been commercially available for more than 40 years. They are extremely versatile, finding applications in many fields in both thermal and ambient cure applications. The present review focuses on their use in the food industry as surface coatings for food and beverage cans, and in particular on their chemical stability in relation to their toxicology and sensorial effects on foods. The implications of these properties of epoxy resins for prospective EU legislation on plastic coatings for food contact is discussed.

Effect of the lactoperoxidase system on lipoprotein lipase activity and lipolysis in milk.

The lactoperoxidase/SCN-/H2O2 system (LPS) was found to inhibit lipoprotein lipase (LPL) in milk. Inhibition was related to the amount of SCN-/H2O2 added to milk. Lipolysis was unaltered until LPL activity was decreased to less than 40% of the original activity. When LPL was inhibited further, decreased lipolysis was observed. Purified LPL was also inhibited by LPS, at similar concentrations of SCN-/H2O2 as in milk. It was shown that non enzymically prepared OSCN- inhibited LPL at concentrations comparable to those produced by the LPS. Cysteine could eliminate the effect of LPS on LPL. The sulphydryl reagents dithiobisnitrobenzoic acid and Na tetrathionate had no effect on LPL activity.

Lipolysis and the distribution of lipase activity in bovine milk in relation to stage of lactation and time of milking.

The increase in levels of free fatty acids (FFA) in morning and afternoon milk after 48 h cold storage at 5 degrees C was determined at two stages of lactation in milk from 96 cows. Lipolysis was positively correlated to day of lactation (r = 0.6, P less than 0.001), while the correlations between lipolysis and milk yield and fat content respectively were due to these factors being related to day of lactation. In afternoon milk the level of FFA increased almost three times above that in morning milk. Lipolysis was closely related to the lipoprotein lipase (LPL) activity associated with the cream fraction (r = 0.8, P less than 0.001). Afternoon milk had higher LPL activity in the cream fraction than morning milk. Lipase activity in the cream increased with increasing stage of lactation. Cooling of milk increased LPL activity associated with the fat phase. This effect was greater in afternoon milk from late lactation than in morning milk from early lactation. When heparin was added to milk the LPL activity associated with the fat increased substantially; again, this effect was greater in afternoon milk from late lactation than in morning milk from early lactation. Lipolysis was higher in heparinized milk than in normal milk, and there was a close correlation between lipolysis and LPL activity associated with the fat (r = 0.82, P less than 0.001). Characteristics of the milk fat globule influencing the attraction of LPL were found to be fundamentally important to lipolysis.

Alkylglycerols in bovine colostrum and milk in relation to precursor levels.

The concentrations of dihydroxyacetone phosphate (DHAP), glycerol-3-phosphate (GP), glucose and alkylglycerols were measured in bovine colostrum and milk. Concentrations of GP were higher in colostrum than in milk, and corresponded to intracellular concentrations at the onset of lactation. This suggests that GP equilibrates over the apical membrane at onset of lactation, which is believed to occur also in full lactation. The ratio of DHAP to GP showed a peak in colostrum that was more than twice that in milk, indicating that concentration changes in colostrum/milk were not caused by dilution. DHAP was positively correlated to metabolical compounds such as glucose and alkylglycerols. As DHAP is a required precursor for alkylglycerol synthesis, the positive correlation suggests that DHAP may be limiting for alkylglycerol synthesis and thus could explain the elevated levels of alkylglycerols found in colostrum.

Incorporation of [hydrogen-3] alkylglycerolether and [carbon-14] hexadecanol into bovine colostrum and milk lipids.

[Hydrogen-3] glycerol ether and [carbon-14] hexadecanol were infused into the mammary gland or jugular vein of cows in colostral or full phases of lactation to determine their relative rates of synthesis and degradation. Neutral alkylglycerols were both synthesized and cleaved in the bovine gland. Oxidation of fatty alcohols and cleaving of neutral alkylglycerol ethers was faster during the milk than the colostral phase of lactation. In the colostral phase, both increased rate of synthesis and decreased cleavage contributed to increased neutral alkylglycerol concentration; however, synthesis changes were greater. Disappearance of [carbon-14] fatty alcohol and [hydrogen-3] alkylglycerol ether from the blood was the magnitude of fatty acid disappearance in previous studies, but uptake by the mammary gland was slower. Alkylglycerols were taken up from the blood and secreted intact into both colostrum and milk.

Incorporation of dietary 1-O-alkyldiacyl glycerols into tissue lipids of neonatal rats.

3H-[9,10]-1-O-alkyl-2,3-diacyl glycerols were administered per os to suckling rats at 1, 3, 6, 9 and 18 days of age. 12 h after administration the animals were killed and the distribution of the labelled material was analysed by whole-body autoradiography. The brown adipose tissue (BAT), intestine and liver showed the highest levels of label at all ages. The lipid content of BAT, intestine and liver were separated into lipid classes, which were analysed for their 3H levels. About 30% of the recovered label was found in the phospholipid fraction at all ages. Little of the administered dose was recovered as alkyl glycerols: 5% in the 1-day-old rat decreasing to less than 1.5% at 18 days of age, indicating that dietary alkyl glycerols only to a very limited degree are incorporated in tissue ether lipids in the young rat.