Sodium Lauryl Sulfoacetate is a safe skin friendly surfactant (foaming agent) for both skin and hair. Sodium Lauryl Sulfoacetate was used in 93 products in 1981, based on voluntary reports provided to FDA by industry; use concentrations ranged from >0.1% to >50%. In 2002 there were 68 uses (FDA 2002) and according to an industry survey in 2004 the current range of use concentrations is 0.6% to 21% (CTFA 2004). Asafety assessment on Sodium Lauryl Sulfoacetatewas published in 1987 with the conclusion “On the basis of the available data presented in this report, the Expert Panel concludes that Sodium Lauryl Sulfoacetate is safe as a cosmetic ingredient in the present practices of use and concentration” (Elder 1987). Studies available since that safety assessment was completed, along with updated information regarding uses and use concentrations, were considered by the CIR Expert Panel. After reviewing the available data, the Panel determined to not reopen this safety assessment.

Mandelic acid is an aromatic alpha hydroxy acid that is used for the treatment of urinary tract infections. The drug is marketed in Canada under the name Mandelamine (as a complex with methenamine). Mandelic acid exerts its antibacterial effect mainly by increasing urine acidity. Moreover, mandelic acid is used as a serum for the treatment of wrinkles.

Acesulfame is a non-nutritive sweetener Acesulfame potassium is a calorie-free artificial sweetener, also known as Acesulfame K or Ace K (K being the symbol for potassium), and marketed under the trade names Sunett and Sweet One. In the European Union, it is known under the E number (additive code) E950. It was discovered accidentally in 1967 by German chemist Karl Clauss at Hoechst AG (now Nutrinova). In chemical structure, acesulfame potassium is the potassium salt of 6-methyl-1,2,3- oxathiazine-4(3H)-one 2,2-dioxide. Acesulfame K has been approved for a variety of uses in more than 90 countries. In 1998, the FDA broadened the US approval of acesulfame K to allow its use in nonalcoholic beverages. It is often blended with sucralose and used to decrease the bitter aftertaste of aspartame. A wide range of low-calorie foods and drinks contain acesulfame K, including table-top sweeteners, chewing gum, jam, dairy products, frozen desserts, drinks and baked goods. Acesulfame K is not broken down when digested, nor is it stored in the body. After being consumed, it is quickly absorbed by the body and then rapidly excreted, unchanged.

Hyaluronic acid (HA) is a high molecular weight biopolysacharide, discovered in 1934, by Karl Meyer and his assistant, John Palmer in the vitreous of bovine eyes. Hyaluronic acid is a naturally occurring biopolymer, which has important biological functions in bacteria and higher animals including humans. It is found in most connective tissues and is particularly concentrated in synovial fluid, the vitreous fluid of the eye, umbilical cords and chicken combs. It is naturally synthesized by a class of integral membrane proteins called hyaluronan synthases, and degraded by a family of enzymes called hyaluronidases. Hyaluronan synthase enzymes synthesize large, linear polymers of the repeating disaccharide structure of hyaluronan by alternating addition of glucuronic acid and N-acetylglucosamine to the growing chain using their activated nucle¬otide sugars (UDP – glucuronic acid and UDP-N-acetlyglucosamine) as substrates. The number of repeat disaccharides in a completed hyaluronan molecule can reach 10 000 or more, a molecular mass of ~4 million daltons (each disaccharide is ~400 daltons). The average length of a disaccharide is ~1 nm. Thus, a hyaluronan molecule of 10 000 repeats could ex¬tend 10 μm if stretched from end to end, a length approximately equal to the diameter of a human erythrocyte. Although the predominant mechanism of HA is unknown, in vivo, in vitro, and clinical studies demonstrate various physiological effects of exogenous HA. Hyaluronic acid possesses a number of protective physiochemical functions that may provide some additional chondroprotective effects in vivo and may explain its longer term effects on articular cartilage. Hyaluronic acid can reduce nerve impulses and nerve sensitivity associated with pain. In experimental osteoarthritis, this glycosaminoglycan has protective effects on cartilage. Exogenous HA enhances chondrocyte HA and proteoglycan synthesis, reduces the production and activity of proinflammatory mediators and matrix metalloproteinases, and alters the behavior of immune cells. In addition to its function as a passive structural molecule, hyaluronan also acts as a signaling molecule by interacting with cell surface receptors and regulating cell proliferation, migration, and differentiation. Hyaluronan is essential for embryogenesis and is likely also important in tumorigenesis. HA plays several important organizational roles in the extracellular matrix (ECM) by binding with cells and other components through specific and nonspecific interactions. Hyaluronan-binding pro¬teins are constituents of the extracellular matrix, and stabilize its integrity. Hyaluronan receptors are involved in cellular signal transduction; one receptor family includes the binding proteins aggrecan, link protein, versican and neurocan and the receptors CD44, TSG6, GHAP and LYVE-1. The chondroprotective effects of hyaluronic acid, e.g., that it stimulates the production of tissue in¬hibitors of matrix metalloproteineses (TIMP-1) by chondrocytes, inhibits neutrophil-mediated cartilage degradation and attenuates IL-1 induced matrix de¬generation and chondrocyte cytotoxicity have been observed in vitro. Articular chondrocytes cultured in the presence of HA have a significantly greater rate of DNA proliferation and ex¬tracellular matrix production, compared with chon¬drocytes cultured without HA.