## 4 Carotenoids Metabolism  
Carotenoids are derived from the general isoprenoid biosynthetic pathway, along with a variety of other important natural substances such as steroids and gibberellic acid. The starting product required to synthetize all the isoprene derivatives is mevalonic acid which is transformed into a phosphorylated isoprene upon phosphorylation; this isoprene subsequently polymerises. In the course of polymerization, the number and position of the double bonds are fixed. The synthesis and degradation of carotennes and xanthophylls, the regulation of carotenogenesis, as well as the role of these compounds, have been very well described in plants [4, 80] and mammals [81]. Multi-gene engineering approaches have also contributed to better understanding of carotenoid metabolism [82]. The conversion of two molecules of geranylgeranyl pyrophosphate (GGPP) to phytoene, a compound common to all C\({}_{40}\) carotenogenic organisms, constitutes the first reaction unique to the carotenoid branch of isoprenoid metabolism. From this step, slightly different reactions can be found in different organisms. Anoxygenic photosynthetic bacteria, non photosynthetic bacteria, and fungi desaturate phytoene either three or four times to yield neurosoprene or lycopene, respectively. In contrast, oxygenic photosynthetic organisms (cyanobacteria, algae, and higher plants) convert phytoene to lycopene via caroten in two distinct sets of reactions. At the level of neurosoprene or lycopene, the carotenoid biosynthesis pathways of different organism's branch to generate the huge diversity of carotenoids found in nature. In photosynthetic organisms and tissues, the lipophilic carotenoid and bacteriochlorophyll (Bchl) or chlorophyll (Chl) pigment molecules associate non-covalently but specifically with integral membrane proteins. In non photosynthetic organisms and tissues, carotenoids, often protein bound, occur in cytoplasmic or cell wall membranes, oil droplets, crystals, and fibrils. As mentioned before, animals are not able to synthesise carotenoids _de novo_. They are acquired throughout the diet. In human beings, it has been well demonstrated that most of the ingested carotenoids are absorbed into the gastrointestinal mucosal cells and appear unchanged in the circulation and tissues. In the intestine, the carotenoids are absorbed by passive diffusion after being incorporated into the micelles that are formed by dietary fat and bile acids. The micellar carotenoids are then incorporated into the chylomicrons and released into the lymphatic system [33]. Carotenoids are transported in the plasma exclusively by lipoproteins. Oxygen-functionalized carotenoids are more polar than carotenes. Thus, \(\alpha\)-carotene, \(\beta\)-carotene and lycopene tend to predominate in low-density lipoproteins (LDL) in the circulation, whereas high-density lipoproteins (HDL) are major carriers of xanthophylls, such as cryptoxanthins, lutein and zeaxanthin. The delivery of carotenoids to extrahepatic tissues is accomplished through the interaction of lipoprotein particles with receptors and the degradation by lipoprotein lipase [83, 84]. Although no less than forty carotenoids are usually ingested in the diet, only six carotenoids and their metabolites have been found in human tissues, suggesting selectivity in the intestinal absorption of carotenoids. In contrast, thirty-four carotenoids and eight metabolites are detected in breast milk and serum of lactating mothers. Recently, facilitated diffusion in addition to simple diffusion has been reported to mediate the intestinal absorption of carotenoids in mammals. The selective absorption of carotenoids may be due to uptake to the intestinal epithelia by means of facilitated diffusion and an unknown mechanism of excretion into the intestinal lumen. It is well known that \(\beta\)-carotene can bemetabolised to vitamin A after intestinal absorption of carotenoids, but little is known about the metabolic transformation of non-provitamin A xanthophylls.