Carotenoids degradation

Insights into the mechanisms of carotenoid degradation can be followed in model systems that are more easily controlled than foods and the formation of initial, intermediate, and final products can also be more easily monitored. However, extrapolation to foods must be done with caution because simple model systems may not reflect the nature and complexity of a multicomponent food matrix and the interactions that can occur. In addition, even in model systems, one must keep in mind that carotenoid analysis and identification are not easy tasks. 

FIGURE 5.3.1 Parts of the isoprenoid pathways to carotenoids. 1 = MEP pathway. 2 = GGPP synthesis. 3 = Carotenoid biosynthetic pathway. 4 = Carotenoid degradative pathways. Enzyme abbreviations and enzyme activities are defined in Table 5.3.1. 

Carmona, M. et al.. Generation of saffron volatiles by thermal carotenoid degradation, J. Agric. Food Chem. 54, 6825, 2006. 

Gandul-Rojas, B., Roca, M., and Mmguez-Mosquera, M.L, Chlorophyll and carotenoid degradation mediated by thylacoid-associated peroxidative activity in olives (Olea europaea) cv. Hojiblanca, J. Plant. Physiol., 161, 499, 2004. 

Esterbauer et al. (1991) have demonstrated that /3-carotene becomes an effective antioxidant after the depletion of vitamin E. Our studies of LDL isolated from matched rheumatoid serum and synovial fluid demonstrate a depletion of /8-carotene (Section 2.2.2.2). Oncley et al. (1952) stated that the progressive changes in the absorption spectra of LDL were correlated with the autooxidation of constituent fatty acids, the auto-oxidation being the most likely cause of carotenoid degradation. The observation that /3-carotene levels in synovial fluid LDL are lower than those of matched plasma LDL (Section 2.2.2) is interesting in that /3-carotene functions as the most effective antioxidant under conditions of low fOi (Burton and Traber, 1990). As discussed above (Section 2.1.3), the rheumatoid joint is both hypoxic and acidotic. We have also found that the concentration of vitamin E is markedly diminished in synovial fluid from inflamed joints when compared to matched plasma samples (Fairburn etal., 1992). This difference could not be accounted for by the lower concentrations of lipids and lipoproteins within synovial fluid. The low levels of both vitamin E and /3-carotene in rheumatoid synovial fluid are consistent with the consumption of lipid-soluble antioxidants within the arthritic joint due to their role in terminating the process of lipid peroxidation (Fairburn et al., 1992). 

The changes that occur after the heat processing of food systems are often monitored by different parameters, such as total carotenoid content (and therefore isomerization and oxidation are underestimated), individual carotenoids (overall changes may be missed), and CIELAB color parameters (no information on carotenoid degradation mechanism). The data given in Table 12.3 reflects the influence of matrix composition, food state (liquid or solid), and measured parameter on the carotenoid degradation kinetics. 

Moreover, carotenoids themselves are very susceptible to oxidative damage and their oxidation products include deleterious aldehydes (Failloux et al., 2003 Hurst et al., 2005 Rozanowski and Rozanowska, 2005 Siems et al., 2000, 2002 Sommerburg et al., 2003). Therefore it is of interest to find out how carotenoids can offer antioxidant protection in cellular systems, how stable the carotenoids are within cells, and what the fate of the carotenoid degradation products is. 

Nucleic acids are not the only biomolecules susceptible to damage by carotenoid degradation products. Degradation products of (3-carotene have been shown to induce damage to mitochondrial proteins and lipids (Siems et al., 2002), to inhibit mitochondrial respiration in isolated rat liver mitochondria, and to induce uncoupling of oxidative phosphorylation (Siems et al., 2005). Moreover, it has been demonstrated that the degradation products of (3-carotene, which include various aldehydes, are more potent inhibitors of Na-K ATPase than 4-hydroxynonenal, an aldehydic product of lipid peroxidaton (Siems et al., 2000). 

Pyranoid monoterpenoid alkaloids have been reviewed, " and halogenated members of this class, (84) and (85), have already been discussed in the halogenated monoterpenoids section. " " The monoterpenoid ether (245) is reported from Artemisia tridentata-, from reported mass spectral data it may well be identical with the previously reported (and uncited) arthole (Vol. 7, p. 20), the characterization of which is still not published. Loliolide (246) is claimed to be an in vivo carotenoid degradation product in Canscora decussata additional spectral data have been published. ... 

Silva Ferreira, A. C., Monteiro, J., Oliveira, C., and Guedes de Pinho, P. (2008). Study of major aromatic compounds in port wines from carotenoid degradation. Food Chem. 110, 83-87. 

Enantioselectivity of Biogenetic Routes. The enantiomeric composition of natural aroma compounds is known to reflect the enantioselectivity of their biogenesis (22). Thus, by elaborating the chiral composition of Cp-norisoprenoids in fruits, we expected to obtain some information about step II m the formation of Ci3-notiso-prenoids, i.e. the enzymatic transformation(s) of the primary carotenoid degradation products into labile aroma precursors (cf. Fig. 3). 

With regard to the metabolism of primary carotenoid degradation p ucts, recent results obtained by Tang and Suga (57) have indicated a two-step mechanism for the conversion of the primary carotenoid metabolite B-ionone 1 to 14 in Nicotiana tabacum plant cells (cf. Fig. 4). These results revealed, that first of all, the side-chain double bond is hydrogenated by the action of carvone reductase (co-factor NADH), before the carbonyl function is enzymatically reduced in the second step. Importantly, the enantioselectivity of the latter reductase is decisive for the enantiomeric composition in fruits as outlined for theaspirane formation from the labile precursor diol 12 (cf. Fig. 5). The formation of vitispiranes 10, edulans 11 and related Ci3-norisoprenoids (29,30) is known to proceed via similar mechanisms. 

Use of Microorganisms for the Bioconversion of Primary Carotenoid Degradation Products. Microbial systems are frequently used for biotransformation... 

An oxidative cleavage of zeaxanthin has been proposed [28] for the formation of carotenoid degradation. 

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