Establishing Standards on Colors from Natural Sources.

Color additives are applied to many food, drug, and cosmetic products. With up to 85% of consumer buying decisions potentially influenced by color, appropriate application of color additives and their safety is critical. Color additives are defined by the U.S. Federal Food, Drug, and Cosmetic Act (FD&C Act) as any dye, pigment, or substance that can impart color to a food, drug, or cosmetic or to the human body. Under current U.S. Food and Drug Administration (FDA) regulations, colors fall into 2 categories as those subject to an FDA certification process and those that are exempt from certification often referred to as "natural" colors by consumers because they are sourced from plants, minerals, and animals. Certified colors have been used for decades in food and beverage products, but consumer interest in natural colors is leading market applications. However, the popularity of natural colors has also opened a door for both unintentional and intentional economic adulteration. Whereas FDA certifications for synthetic dyes and lakes involve strict quality control, natural colors are not evaluated by the FDA and often lack clear definitions and industry accepted quality and safety specifications. A significant risk of adulteration of natural colors exists, ranging from simple misbranding or misuse of the term "natural" on a product label to potentially serious cases of physical, chemical, and/or microbial contamination from raw material sources, improper processing methods, or intentional postproduction adulteration. Consistent industry-wide safety standards are needed to address the manufacturing, processing, application, and international trade of colors from natural sources to ensure quality and safety throughout the supply chain.

Photo- and thermodegradation of anthocyanins from grape and purple sweet potato in model beverage systems.

Recently, interest in the application of natural pigments to replace synthetic dyes in beverages has grown. The present study investigates the stability of anthocyanin-rich grape and purple sweet potato (PSP) extracts to photo- and thermostresses in ready-to-drink (RTD) beverage models including hot fill beverages with various concentrations of ascorbic acid, a preserved beverage, and a vitamin-enriched water beverage. Thermo- and photostresses were induced at 40, 60, and 80 °C and 250, 500, and 750 W/m(2), respectively. Qualitative and quantitative data on anthocyanin content were collected by pH differential assay and LC-MS. Increasing concentration of ascorbic acid caused more rapid degradation through thermostress, but had a protective effect through photostress. Additionally, PSP was significantly less stable than grape extract in the vitamin-enriched water model beverage through photostress. Furthermore, photostress caused the formation of monoacylated peonidins from diacylated peonidins.

Activation of extracellular signal-regulated kinase is involved in mechanical strain inhibition of RANKL expression in bone stromal cells.

Mechanical input is known to regulate skeletal mass. In vitro, application of strain inhibits osteoclast formation by decreasing expression of the ligand RANKL in bone stromal cells, but the mechanism responsible for this down-regulation is unknown. In experiments here, application of 1.8% equibiaxial strain for 6 h reduced vitamin D-stimulated RANKL mRNA expression by nearly one-half in primary bone stromal cells. Application of strain caused a rapid activation of ERK1/2, which returned to baseline by 60 minutes. Adding the ERK1/2 inhibitor PD98059 30 minutes before strain delivery prevented the strain effect on RANKL mRNA expression, suggesting that activation of ERK1/2 was required for transduction of the mechanical force. Mechanical strain also activated N-terminal Jun kinase (JNK) that, in contrast, did not return to baseline during 24 h of continuous strain. This suggests that JNK may represent an accessory pathway for mechanical transduction in bone cells. Our data indicate that strain modulation of RANKL expression involves activation of MAPK pathways.