Plasma, carotene vitamin

Vitamin C levels can be determined in stored blood or blood components such as serum, plasma, or leukocytes if particular preservation steps are performed during preparation. The concentration of vitamin C is stable in whole blood for several hours with negligible decay. If whole blood is centrifuged and serum or plasma obtained, vitamin C starts to disappear immediately. Therefore, the stabilization of vitamin C by metaphosphoric acid or other substances is required if such aliquots are to be used to determine vitamin C concentration in future analyses. The need for preserving aliquots is unnecessary in the determination of other antioxidant substances such as vitamin E or carotenoids. The preservation issue may also be a reason that blood determinations of antioxidants, such as (3-carotene or vitamin E, and their relation to disease risk are found more frequently than vitamin C (Comstock a/., 1992). 

Plasma Concentrations of Vitamin A, Vitamin E, -Carotene, Vitamin C, and Selenium and Activity of Glutathione Peroxidase (GSH-Px) in Red Blood Cells of Cystic Fibrosis Patients with (CF + ) and without (CF-) Chronic Inflammation... 

Gey, K.F. et al.. Poor plasma status of carotene and vitamin C is associated with higher mortality from ischemic heart disease and stroke Basel Prospective Study, J. Clin. Invest., 71, 3, 1993. 

Lindqvist, A. and Andersson, S., Biochemical properties of purified recombinant human beta-carotene 15,15-monooxygenase, J. Biol. Chem., 277, 23942, 2002. Krinsky, N.I., Cornwell, D.G., and Oncley, J.I., The transport of vitamin A and carotenoids in human plasma. Arch. Biochem. Biophys., 73, 233, 1958. 

The lag-phase measurement at 234 nm of the development of conjugated dienes on copper-stimulated LDL oxidation is used to define the oxidation resistance of different LDL samples (Esterbauer et al., 1992). During the lag phase, the antioxidants in LDL (vitamin E, carotenoids, ubiquinol-10) are consumed in a distinct sequence with a-tocopherol as the first followed by 7-tocopherol, thereafter the carotenoids cryptoxanthin, lycopene and finally /3-carotene. a-Tocopherol is the most prominent antioxidant of LDL (6.4 1.8 mol/mol LDL), whereas the concentration of the others 7-tocopherol, /3-carotene, lycopene, cryptoxanthin, zea-xanthin, lutein and phytofluene is only 1/10 to 1/300 of a-tocopherol. Since the tocopherols reside in the outer layer of the LDL molecule, protecting the monolayer of phospholipids and the carotenoids are in the inner core protecting the cholesterylesters, and the progression of oxidation is likely to occur from the aqueous interface inwards, it seems reasonable to assign to a-tocopherol the rank of the front-line antioxidant. In vivo, the LDL will also interact with the plasma water-soluble antioxidants in the circulation, not in the artery wall, as mentioned above. 

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). 

Orlistat reduces the absorption of fat-soluble vitamins. Daily intake of a multivitamin containing vitamins A, D, E, and K, as well as 3-carotene, is recommended. Patients should take the multivitamin 2 hours prior to or after the dose of orlistat.31 Since availability of vitamin K may decline in patients receiving orlistat therapy, close monitoring of coagulation status should occur with concomitant administration of warfarin.31 Administration of orlistat in conjunction with cyclosporine can result in decreased cyclosporine plasma levels. To avoid this interaction, cyclosporine should be taken 2 hours preceding or following the dose of orlistat. Additionally, cyclosporine levels should be monitored more frequently.31... 

Carotene (all-trans), (3-cryptoxanthin (all-trans and -cis), zeaxanthin (all-trans), luteoxanthin isomers, violaxanthin (all-trans and -cis), and neoxanthin (all-trans and -cis) were identified in several mango cultivars (Mercadante and others 1997 Ornelas-Paz and others 2007, 2008). Mango retinol was found to be highly bioavail-able by estimating vitamin A and carotene reserves in the liver and plasma of rats. Information on the tocopherol content in mango is very scarce, but it seems to be low (Burns and others 2003 Ornelas-Paz and others 2007). 

Fresh tomato fruit contains about 0.72 to 20 mg of lycopene per 100 g of fresh weight, which accounts for about 30% of the total carotenoids in plasma (Stahl and Sies 1996). In contrast to other pigments such as (3-carotene, lutein, violaxanthin, auroxanthin, neoxanthin, and chlorophylls a and b, which accumulate in inner pulp and in the outer region of the pericarp, lycopene appears only at the end of the maturation period and almost exclusively in the external part of the fruit (Laval-Martin and others 1975). Other tomato components that can contribute to health include flavonoids, folic acid, and vitamin E (Dorais and others 2001a,b). 

The possible involvement of free radicals in the development of hypertension has been suspected for a long time. In 1988, Salonen et al. [73] demonstrated the marked elevation of blood pressure for persons with the lowest levels of plasma ascorbic acid and serum selenium concentrations. In subsequent studies these authors confirmed their first observations and showed that the supplementation with antioxidant combination of ascorbic acid, selenium, vitamin E, and carotene resulted in a significant decrease in diastonic blood pressure [74] and enhanced the resistance of atherogenic lipoproteins in human plasma to oxidative stress [75]. Kristal et al. [76] demonstrated that hypertention is accompanied by priming of PMNs although the enhancement of superoxide release was not correlated with the levels of blood pressure. Russo et al. [77] showed that essential hypertension patients are characterized by higher MDA levels and decreased SOD activities. 

Recently we published data that even in countries with excellent food sources and availability, insufficient vitamin A supply will occur (Schulz et ah, 2007). The aim of this trial was to analyze vitamin A and p-carotene status and investigate the contribution of nutrition to vitamin A and p-carotene supply in mother-infant pairs of multiparous births or births within short birth rates. Twenty-nine volimteers aged between 21 and 36 years were evaluated for 48 hours after delivery. In order to establish overall supply, retinol and p-carotene were determined in maternal plasma, cord blood, and colostrum via HPLC analysis. A food frequency protocol was obtained from all participants. Regardless of the high-to-moderate socioeconomic background, 27.6% of participants showed plasma retinol levels below 1.4 pmol/liter, which can be taken as borderline deficiency. In addition, 46.4% showed retinol intake <66% of RDA and 50.0% did not consume liver at all, although liver contributes as a main source for preformed retinol. Despite a high total carotenoid intake of 6.9 3.9mg/day, 20.7% of mothers showed plasma levels <0.5 pmol/liter p-carotene. 

Retinol and p-carotene levels were highly significant correlated between maternal plasma versus cord blood and colostrum. In addition, significantly lower levels were found in cord blood [31.2 13% (retinol), 4.1 1.4% (p-carotene)] compared with maternal plasma. Despite the fact that vitamin A- and p-carotene-rich food is generally available, in contrast to developing countries, risk groups for low vitamin A supply indeed exist in the western world. 

In the body retinol can also be made from the vitamin precursor carotene. Vegetables like carrots, broccoli, spinach and sweet potatoes are rich sources of carotene. Conversion to retinol can take place in the intestine after which retinyl esters are formed by esterifying retinol to long chain fats. These are then absorbed into chylomicrons. Some of the absorbed vitamin A is transported by chylomicrons to extra-hepatic tissues but most goes to the liver where the vitamin is stored as retinyl palmitate in stellate cells. Vitamin A is released from the liver coupled to the retinol-binding protein in plasma. 

The role of the antioxidant properties of vitamins C, E, and p-carotene in the prevention of cardiovascular disease has been the focus of several recent studies. Antioxidants reduce the oxidation of low-density lipoproteins, which may play a role in the prevention of atherosclerosis. However, an inverse relationship between the intake or plasma levels of these vitamins and the incidence of coronary heart disease has been found in only a few epidemiological studies. One study showed that antioxidants lowered the level of high-density lipoprotein 2 and interfered with the effects of lipid-altering therapies given at the same time. While many groups recommend a varied diet rich in fruits and vegetables for the prevention of coronary artery disease, empirical data do not exist to recommend antioxidant supplementation for the prevention of coronary disease. 

Vitamin A absorption from the small intestine requires dietary fat and pancreatic lipase to break down retinyl esters and bile salts to promote the uptake of retinol and carotene. Drugs, such as mineral oil, neomycin and cholestyramine, that can modify lipid absorption from the gastrointestinal tract can impair vitamin A absorption. The use of oral contraceptives can signihcantly increase plasma vitamin A levels. 

Dietary carotenes and carotenoids are absorbed and transported in the plasma of humans and animals by lipoproteins.149 Tire conversion of carotenes to vitamin A (Box 22-A) provides the aldehyde retinal for synthesis of visual pigments (Chapter 23) and retinoic acid, an important regulator of gene transcription and development (Chapter 32).150 152c See also Section E,5. 

Another important field of application concerns food and beverages, especially wine, juices, and tea (A2, A11, A17, B4, K12, V7, Yl). The antioxidant components of food include vitamin E (a-tocopherol), vitamin A (retinoids), vitamin C (ascorbic acid), and also fi-carotene (provitamin A), other carotenoids (of which more than 600 compounds have been identified), flavonoids, simple phenols, and glucobrasicins (H3). Unfortunately, the TAC value of a food is not informative on the bioavailability of its antioxidants. It has been estimated that polyphenols are normally present in blood plasma at concentrations of 0.2-2 //M (PI). However, it has been demonstrated that feeding rats a quercetin-augmented diet can increase their plasma levels of quercetin and its metabolites up to 10-100 //M (M27), and transient increases in the concentration of plant-derived phenolic compounds can take place after ingestion of food and beverages, which may affect blood plasma TAC (see later). 

In the intestinal mucosal cells, /3-carotene is cleaved via an oxygenase (an enzyme that introduces molecular 02 into organic compounds) to frans-retinal (aldehyde form of trans-retinol, as shown in Table 6.2), which in turn is reduced to frans-retinol, vitamin Av Retinol is then esterified with a fatty acid, becomes incorporated into chylomicrons, and eventually enters the liver, where it is stored in the ester form until it is required elsewhere in the organism. The ester is then hydrolyzed, and vitamin Ax is transported to its target tissue bound to retinol-binding protein (RBP). Since RBP has a molecular weight of only 20,000 and would be easily cleared by the kidneys, it is associated in the bloodstream with another plasma protein, prealbumin. 

Gey, K.F., Moser, U.K., Jordan, P., Stahelin, H.B., Eicholzer, M., Lundin, E. 1993. Increased risk of cardiovascular disease at suboptimal plasma concentrations of essential antioxidants an epidemiological update with special attention to (3-carotene and vitamin C. Am. J. Clin. Nutr. 57, 787S-797S. 

The oxidative modification of LDL has been implicated in atherosclerosis. This disease may be regarded as a chronic inflammatory condition, and here we discuss how oxidatively modified LDL (oLDL) may play a role not only in atherosclerosis but also in other chronic inflammatory diseases such as RA. LDL (Mr = 2.5 x 106) is one of the major plasma carriers of lipids, as well as the antioxidants vitamin E and (3-carotene. Because of its high content of unsaturated fatty acids, LDL is uniquely sensitive to lipid peroxidation [ 117]. 

---