Hyaluronic acid protein content

The lower degree of polymerization of hyaluronic acid present in rheumatoid fluids (B3, BIO, B13, B18) undoubtedly impairs the effectiveness of the fluid as a lubricant between joints. Another factor contributing to this may be the lower concentration of hyaluronic acid found in certain rheumatoid effusions. Special viscosity and elastic properties are exhibited by hyaluronic acid in synovial fluid in concentrations in excess of 0.2 g/lOO ml (Bll) the concentration of hyaluronic acid in inflamed joint fluids of rheumatoid arthritis is generally less than this value. In a recent investigation, Hamerman and Sandson (H4) found that, apart from a reduced anomalous viscosity, the hyaluronate-protein complexes of synovial fluid differed from normal and showed increases in both protein content and amounts of basic amino acids. 

This disease is of considerable interest in relation to oxypurine metabolism, although a wide variety of potential metabolic abnormalities have been said to be associated with it. In a review in 1961 Tickner (T4) asserted that there was evidence to support the postulate that psoriasis was associated with alterations in lipid, protein, carbohydrate, and mineral metabolism as well as in serum protein level. Investigators have since supported a myriad of hypotheses. Note has been taken of variations in carbohydrate metabolism (R16), and of changes in the synthesis of hyaluronic acid with resultant alterations in transport mechanisms (CIO). Changes in fatty acid levels and metabolism (C8), alterations of aldolase activity (C6), increased proteolytic activity (S33), and alterations in the composition of proteins in psoriatic scales (L20) have been suggested. Changes in serum copper content in psoriatic patients have been observed (L18). 

The current method for the hyaluronidase assay described in the United States Pharmacopeia (USP) [132] is based on the inability of hydrolyzed potassium hyaluronate to form a complex precipitate with proteins from added serum, reflected in a decreased turbidity of the reaction mixture (measured after 30 min). The method is, from the enzymological point of view, not well defined since it does not actually evaluate the kinetics of the hydrolysis of the substrate. An assay with end-point determination is only valid if the reaction rate does not change during this reaction time. We found that only with the two lowest test concentrations (0.15 and 0.3 IU) was this condition fulfilled, while with the three higher test concentrations the reaction is not linear. Commercially available hyaluronates can be contaminated with chondroitin sulfates. They are more acidic than hyaluronic acid itself and hence can form better protein complexes and influence the turbidity. In a suitability test of the USP [133], the substrate must pass both an inhibitor content test and a turbidity-production test. The assumption is made that... 

The function of hyaluronic acid was initially confined to the maintenance and sta-bihty of the ECM (96). However, the action of hyaluronic acid varies with its size, which determines its function in a cell-type specific manner (97-101). Hyaluronic acid represents more than 50% of the ECM in the skin. High molecular weight hyaluronic acid (>1,000 kDa) controls tissue water content, ECM lubrication, structural integrity, free oxygen radicals, and distribution of plasma proteins (96,100,101). The synthesis of hyaluronic acid is achieved by hyaluronan synthase-1 to -3 (102,103). The stability of hyaluronic acid varies with its microenvironment, as its half-life is less than 10 min in blood, up to 12 h in the skin, and extends to months in the vitreous gel of the eye (100,101). Hyaluronic acid is the only GAG with a function of its breakdown molecules, as small hyaluronic acid molecules and fragments stimulated the maturation of dentritic cells and the synthesis of proinflammatory IL-lp, IL-12, and TNF-a (103-105). The latter effect seems to be restricted to an interaction of hyaluronic acid fragments with the Toll-like receptor 4 (104,105). The observation that bacterial spreading in the... 

The urinary excretion of glycosaminoglycans by juvenile cases of vitamin A deficiency and of protein-calorie malnutrition (kwashiorkor) is less than normal (M41). The predominant differences are the absence of hyaluronic acid and the presence of chondroitin sulfate of low sulfate content (C12). Treatment of the cases with vitamin A deficiency restored the glycosaminoglycan spectrum to normal. Decreased urinary glycosaminoglycan levels have also been noted in primary hepatoma (K6). It has been suggested that the urinary excretion pattern of individual glycosaminoglycans is pathognomic of certain hereditary bone diseases (T3). 

The proteoglycans contain heteropolysaccharides known as glycosaminoglycans, an unwieldy term that emphasizes their content of hexosamines and uronic acids. Formerly glycosaminoglycans were known as mucopolysaccharides. The best known members of this group are the chondroitin sulphates and hyaluronic acid. Though they are characterized by the structure of their polysaccharide chains, these are almost invariably associated with protein, hence the term proteoglycan. 

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