Carotenoids mechanism

Kolaczkowski (1989) incorporated perdeutero-spheroidene into protonated and deuterated RCs and explored the role of vibrational terms in the mechanism of triplet enagy transfer from the primary donor to the carotenoid. Mechanisms of triplet energy transfer have been postulated to involve specific electronic and/or vibrational states and/or structural changes in the protein to account for the activated nature of the process (Frank et al., 1983, 1993a, 1996 Takiff and Boxer, 1988a,b Kolaczkowski, 1989 Fous and Hoff, 1989). 

The complex nature of the mass transfer of carotenoids to absorbable lipid species, the diversity of raw and processed foods consumed, and individual variations in the degree of mastication, will lead to differences in the amount of carotenoid that becomes bioaccessible and potentially available for absorption. By understanding the underlying mechanisms of these processes, for a wider range of fruit and vegetable constituents, it will become possible... 

A small but variable proportion of the carotenoids with one or two P-ionone rings (mainly P-carotene) are cleaved in the enterocytes to produce retinol (vitamin A). This process is very tightly controlled, so that too much vitamin A is not produced, although the control mechanism is not clear. Some cleavage of P-carotene can also occur in the liver, but this does not account for the turnover of P-carotene in the body. Small amounts of carotenoids are subject to enterohepatic circulation, but this does not account for losses. 

The mechanisms of the metabolism and excretion of P-carotene are not clear, other than the identification of a number of partially oxidised intermediates found in plasma (Khachik et al., 1992). It is assumed that the carotenoids are metabolised in a manner analogous to the P-oxidation of fatty acids although there is no evidence for this. 

Clearly, the control of gene expression at the transcriptional level is a key regulatory mechanism controlling carotenogenesis in vivo. However, post-transcriptional regulation of carotenoid biosynthesis enzymes has been found in chromoplasts of the daffodil. The enzymes phytoene synthase (PSY) and phytoene desaturase (PDS) are inactive in the soluble fraction of the plastid, but are active when membrane-bound (Al-Babili et al, 1996 Schledz et al, 1996). The presence of inactive proteins indicates that a post-translational regulation mechanism is present and is linked to the redox state of the membrane-bound electron acceptors. In addition, substrate specificity of the P- and e-lycopene cyclases may control the proportions of the p, P and P, e carotenoids in plants (Cunningham et al, 1996). 

The carotenoid pathway may also be regulated by feedback inhibition from the end products. Inhibition of lycopene cyclisation in leaves of tomato causes increase in the expression of Pds and Psy-1 (Giuliano et al, 1993 Corona et al, 1996). This hypothesis is supported by other studies using carotenoid biosynthesis inhibitors where treated photosynthetic tissues accumulated higher concentrations of carotenoids than untreated tissues (reviewed by Bramley, 1993). The mechanism of this regulation is unknown. A contrary view, however, comes from studies on the phytoene-accumulating immutans mutant of Arabidopsis, where there is no feedback inhibition of phytoene desaturase gene expression (Wetzel and Rodermel, 1998). 

CUNNINGHAM F X Jr, POGSON B, SUN Z, MCDONALD K A, DELLAPENNA D and GANTT E (1996) Functional analysis of the (3 and e lycopene cyclase enzymes of Arabidopsis reveals a mechanism for control of cyclic carotenoid formation . Plant Cell, 8, 1613-26. 

Elliot, R., Mechanisms of genomic and non-genomic actions of carotenoids, Biochim. Biophys. Acta Molecular Basis Dis., 1740, 147, 2005. 

The hypothesis of the participation of those cholesterol transporters (NPCILI and ABCAl) in the carotenoid transport remains to be confirmed, especially at the in vivo human scale. If the mechanism by which carotenoids are transported through the intestinal epithelial membrane seems better understood, the mechanism of intracellular carotenoid transport is yet to be elucidated. The fatty acid binding protein (FABP) responsible for the intracellular transport of fatty acids was proposed earlier as a potential transporter for carotenoids. FABP would transport carotenoids from the epithelial cell membrane to the intracellular organelles such as the Golgi apparatus where CMs are formed and assembled, but no data have illustrated this hypothesis yet. 

The ability of carotenoids to act as antioxidants is closely related to their long-chain conjugated polyene structures (see Section 2.2 in Chapter 2). Two main types of antioxidant actions can be distinguished singlet oxygen quenching and reactions with radicals. The first mechanism occurs in vivo in plants and has been extensively studied in vitro. Reactions with radicals of different types have also been extensively studied in vitro under different conditions but their occurrence in vivo is still a matter of discussion. 

Carotenoid chemical structure is usually not affected by the physical quenching. Another mechanism can occur in which a carotenoid chemically quenches singlet oxygen and is thus transformed in derived products. ... 

Experimental evidence in humans is based upon intervention studies with diets enriched in carotenoids or carotenoid-contaiifing foods. Oxidative stress biomarkers are measured in plasma or urine. The inhibition of low density lipoprotein (LDL) oxidation has been posmlated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Since carotenoids are transported mainly via LDL in blood, testing the susceptibility of carotenoid-loaded LDL to oxidation is a common method of evaluating the antioxidant activities of carotenoids in vivo. This type of smdy is more precisely of the ex vivo type because LDLs are extracted from plasma in order to be tested in vitro for oxidative sensitivity after the subjects are given a special diet. 

In atherosclerosis and other heart diseases, the role of carotenoids as antioxidants is probable, but for these types of diseases and also for other degenerative diseases such as cancers, non-antioxidant activities constitute other possible prevention mechanisms. These activities are, for example, stimulation of gap junction communications between cells, and the induction of detoxifying enzymes. The... 

Two main mechanisms by which a carotenoid can become a prooxidant have been proposed and reviewed ... 

Studies on carotenoid autoxidation have been performed with metals. Gao and Kispert proposed a mechanism by which P-carotene is transformed into 5,8-per-oxide-P Carotene, identified by LC-MS and H NMR, when it is in presence of ferric iron (0.2 eq) and air in methylene chloride. The P-carotene disappeared after 10 min of reaction and the mechanism implies oxidation of the carotenoid with ferric iron to produce the carotenoid radical cation and ferrous iron followed by the reaction of molecular oxygen on the carotenoid radical cation. Radical-initiated autoxidations of carotenoids have also been studied using either radical generators like or NBS.35... 

In conclusion, oxidation of carotenoids by molecular oxygen, the so-called autoxidation process, is a complex phenomenon that is probably initiated by an external factor (radical, metal, etc.) and for which different mechanisms have been proposed. The autoxidation of a carotenoid is important to take into account when studying antioxidant activity because it can lower the apparent antioxidant activity of a carotenoid. ... 

FIGURE 3.3.2 Hypothesized mechanism of formation of lycopene oxidation products in an abiotic system. The compound numbers correspond to those cited in Britton, G. et ah, Carotenoids HandbookP... 

The ready availability of carotenoid oxidation products through chemical methods will facilitate their use as standard identification tools in complex media such as biological fluids, and enable in vitro investigation of their biological activity. Moreover, these studies can help reveal the mechanisms by which they can be chemically or biochemically cleaved in vivo. 

The underlying mechanisms involved in the activities of carotenoid oxidation products are due either to a possible role as precursors of retinoids that would be the active species for positive effects or to their own specific activities. This latter case is illustrated by the activity of non-provitamin A carotenoid oxidation products such as those derived from lycopene. However, biological effects of carotenoid oxidation products other than retinoids are only hypothesized in vivo in humans, which hypothesis has been used as the basic principle to justify in vitro studies of these compounds. 

Carotenoid oxidation products are also supposed to have detrimental effects in vivo. As mentioned earlier, they are suspected to be involved in the adverse effects of high doses of 3-carotene supplementation in smokers and asbestos workers (CARET and ATBC studies) and in smoke-exposed ferrets. The mechanisms potentially involved have been investigated in vitro. P-Apo-8 -carotenal, an eccennic cleavage oxidation product of P-carotene, was shown to be a strong inducer of CYPlAl in rats, whereas P-carotene was not active. Cytochrome P450 (CYP 450) enzymes thus induced could enhance the activation of carcinogens and the destruction of retinoic acid. ... 

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. 

Kanasawud, P. and Crouzet, J.C., Mechanism of formation of volatile compounds by thermal degradation of carotenoids in aqueous medium. 1. (3-Carotene degradation, J. Agric. Food Chem., 38, 237, 1990. 

Scotter, M.J., Characterization of the coloured thermal degradation products of bixin from annatto and a revised mechanism for their formation, Food Chem., 53, 111, 1995. Zechmeister, L., Cis-trans isomerization and stereochemistry of carotenoids and diphenylpolyenes, Chem. Rev., 34, 267, 1944. 

For the sake of study, the biosynthesis of carotenoid plant pigments can be divided into parts involving enzymes and their associated activities as listed in Table 5.3.1 and further detailed in Figure 5.3.1 through Figure 5.3.4. Some of the parts have common enzymatic mechanisms and may also be in distinct subcellular compartments such as cytoplasm, endoplasmic reticulum, or plastid thylakoid. 

The stability of phytoene desaturase and lycopene cyclase transcripts also influenced accumulation of carotenoids. Efforts in directed evolution of carotenogenic enzymes have also continued. Alternate approaches using systematic and combinatorial gene knockout targets have allowed for enhancement of carotenoid production in the absence of a priori assumptions of regulatory mechanisms. 

Understanding mechanisms controlling metabolon localization in plastids of different membrane architectures Little is known about metabolon structure, assembly, and membrane targeting. The carotenoid biosynthetic pathway exists on plastid membranes. However, plastids have different membrane architectures and therefore tissue- and plastid-specific differences in membrane targeting of the biosynthetic metabolon can be expected. Localization in chloroplasts that harbor both thylakoid and envelope membranes differs from the envelope membranes in endosperm amy-loplasts. In fact, localization on both thylakoid and envelope membranes implies that the carotenoid pathway is really not a single pathway, but a duplicated pathway that may very well have membrane-specific roles with regard to functions in primary and secondary metabolism. 

Little is known of how the biosynthetic metabolon is assembled, what mechanisms control the membrane-specific targeting, and how the conversions to apocarotenoids occur. Yet the current approach to drive import of bacterial or plant genes is to use transit sequences of a stromal protein that may limit the effectiveness of the transgene. In addition, for specific applications of controlling carotenoid composition, we need to better understand the interactions of the various enzymes,... 

Considering that each stationary phase has a different mechanism of separation, the analyst should apply the most suitable phase for a particular carotenoid separation, not forgetting that it is very useful to look for previous experiences among the several examples available in the literature and that it is also possible to find different solutions for the same problem. 

NPQ (Rakhimberdieva et al. 2004) exactly matches the absorption spectrum of the carotenoid, 3 -hydrox yech i nenone (Polivka et al. 2005) in the OCP. The OCP is now known to be specifically involved in the phycobilisome-associated NPQ and not in other mechanisms affecting the levels of fluorescence such as state transitions or D1 damage (Wilson et al. 2006). Studies by immunogold labeling and electron microscopy showed that most of the OCP is present in the interthylakoid cytoplasmic region, on the phycobilisome side of the membrane, Figure 1.2 (Wilson et al. 2006). The existence of an interaction between the OCP and the phycobilisomes and thylakoids was supported by the co-isolation of the OCP with the phycobilisome-associated membrane fraction (Wilson et al. 2006, 2007). 

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