Brown pigment formation

FIGURE 11.13 Effect of temperature on brown pigment formation model system (G, glucose F, fructose Gin, glutamine). 

FIGURE 11.14 Influence of water activity on HMF accumulation and brown pigment formation in orange juice concentrate at 45°C for 48 days. 

Eichner, K. and Karel, M. The influence of water content and water activity on brown pigment formation, /. Agric. Food Chem., 20, 218, 1972. 

Eichner, K. The influence of water content on brown pigment formation in dehydrated foods and model systems and the inhibition of fat oxidation by browning intermediates, in Water Relations of Foods, Duckworth, R.B., Ed., Academic Press, New York, 1975, p. 417. 

Armstrong attributed the increased resistance of dentin matrix to proteolysis to the blockage of susceptible sites by covalently bound carbohydrate. Later it became clear that the Maillard reaction induces the formation of covalent bonds (cross-links) between protein molecules, accounting for such resistance as well. The presence of non-degradable matrix proteins inhibits mineral dissolution (Chapter 2). In addition, both brown pigments and cross-linked proteins inhibit the production of extracellular polysaccharides by cariogenic streptococci (Kobayashi et al., 1990). 

The formation of brown pigments via the Maillard reaction, especially in model systems (e.g. glucose-glycine), usually follows zero-order kinetics, but the loss of reactants has been found to follow first- or second-order kinetics in foods and model systems. Activation energies of 109, 116 and 139 kJ mol-1 have been reported for the degradation of lysine, the formation of brown pigments and the production of hydroxymethylfurfural (HMF), respectively. 

Skin problems can be persistent in a proportion of patients, variously estimated at 10-59%, and this can severely limit adherence to therapy. The skin reaction can be ameliorated by concomitant use of non-steroidal anti-inflammatory drugs such as aspirin and indometacin (SEDA-15, 412). Transient exanthems, pruritus, and sometimes wheals are seen, as well a uniform dryness and scaling of the epidermis, brown pigmentation, and even on occasion an acanthosis nigricans-like dermatosis (15). Persistent rashes can also occur. Doses in excess of 5 g/day are routinely associated with skin manifestations and can on occasion cause liver damage, gout and ulcer formation. These reactions can be associated with nicotinic acid rather than nicotinamide, which is sometimes recommended as an alternative (37). Increased hair loss has been described. 

Lipid oxidation products react with proteins and other amino compounds to form brown substances, similar to melanoidins. The formation of such brown substances was reviewed already at the first Maillard Symposium.150 The pigments formed are partly soluble in chloroform-methanol and partly insoluble, whereas true melanoidins are largely water-soluble. As most brown pigments of fish muscle are soluble in benzene-methanol and only to a lesser extent in water, the implication is that here oxidised lipid-protein interactions are more important than Maillard browning due to ribose-amino acid interactions. 

Maillard reaction. The reaction of amino groups of amino acids, peptides, or proteins with the glycosidic hydroxyl group of sugars resulting in the formation of brown pigments. Also known as the Browning reaction. 

The first two steps in the synthesis of melanin are catalyzed by tyrosinase, a copper-containing oxidase, which converts tyrosine to dopaquinone. All subsequent reactions presumably occur through nonenzymatic auto-oxidation, in the presence of zinc, with formation of the black to brown pigment eumelanin. The yellow to reddish brown, high-molecular-weight polymer known as pheomelanin and the low-molecular-weight trichromes result from addition of cysteine to dopaquinone and further modification of the products. Pheome-lanins and trichromes are primarily present in hair and feathers. 

No detailed studies of tannins in bacterial infected cotton have been made. However, the formation of dark brown pigments is a part of the necrogenic response to X. campestris. Brown pigments in cotton have been shown to originate from oxidation of tannins (27, 64), most of which have been newly synthesized in diseased tissue TT)5). Yenere (62) found a marked increase in extractable peroxidase activity in resistant but not susceptible tissue in response to X. campestris, and mixtures of peroxidase and catechin (a monomeric unit... 

The formation of post-Amadori glycosylation rearrangement products and yellow-brown pigments is a reflection of normal blood glucose concentra-... 

L-ascorbic acid (AA) and its isomer D-erythorbic acid (EA) (also called D-isoascorbic acid) have been used as inhibitors of enzymatic browning in fruit and vegetable products for at least 50 years, (15-17). These compounds prevent quinone accumulation and subsequent pigment formation by reducing the 0-quinones generated from the phenolic substrates of PPO back to O-dihydroxyphenolic compounds (17-18). AA also can act as a PPO inhibitor (19-20). AA and EA are used interchangeably although there are indications that AA is more effective in some systems (21-22). 

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