Antioxidant in blood

Olas B and Wachowicz B. 2002. Resveratrol and vitamin C as antioxidants in blood platelets. Thromb Res 106(2) 143-148. 

A large number of reports on the biological activity of antioxidants in blood plasma and cell membranes verify that vitamin E (VE) is the most significant... 

Figure 10 Lipid-soluble antioxidants in blood plasma in rabbits fed 4 weeks with probu-col and two newly synthesized compounds. All products were administered in equal amounts. The VE portion is the dark gray portion of the columns. Contr., control group Prob., group fed with probucol S-1 and S-2, groups fed with new antioxidants.

Terao, J., Murota, K., and Moon, J.-H., Quercetin glucosides as dietary antioxidants in blood plasma modulation of their function by metabolic conbversion, in Free Radicals in Chemistry, Biology and Medicine, Yoshikawa, T., Toyokuni, Y., Yamamoto, Y., and Naito, Y., Eds., OIAC International, London, 2000, p. 50. 

The contribution of lipophilic antioxidants is small. Escobar et al. (E5) found that the TAC of lipophilic antoxidants in blood plasma was 16.5 1.5 pM and corresponded almost exclusively to a-tocopherol the concentration of this compound in the blood plasma, analyzed independently, was 17.6 0.3 pM. Popov and Lewin (PI9) found TAC of lipid-soluble antioxidants in blood plasma to be 28.0 8.1 /u.M, a value comparable with the concentration of a-tocopherol (20.5 6.6 /U.M). These (and other) results confirm that a-tocopherol is the main lipid-soluble antioxidant of blood plasma (II) and indicates that the contribution of the lipid-soluble antioxidants to TAC of blood plasma is in fact negligible, taking into account that TAC of human blood plasma is of the order of 1 mM (see later). The contribution of ascorbic acid is also low. This situation may differ considerably in other biological fluids and tissue homogenates. In seminal plasma, the concentration ratio of ascorbate to urate is about 1 (G3). Ascorbate and urate contribute 29% of the fast TRAP of human seminal plasma the share of proteins and polyphenolic compounds is 57%, whereas tyrosine contributes 15% of the slow TRAP (R14) (Table 7). Ascorbate and uric acid account for about half of TAC of human tears (K3). TAC of urine is determined mainly by urate and proteins (K5). 

E5. Escobar, J., Cardenas, G., and Lissi, E. A., Evaluation of the total content of lipid-soluble antioxidants in blood plasma samples employing a simple chemiluminescence quenching procedure. J. Biochem. Biophys. Meth. 35, 57-60 (1997). 

Flavonoids are used in treatment of many diseases, mainly because of their capability to inhibit many harmful strains of bacteria and enzymes (proteases, reverse transcriptase), to stimulate hormones and neurotransmitters, and to capture free radicals (Havsteen 2002). There are reports confirming that supplementation of diet with an antioxidant (a-tocopherol), by increasing the concentration of the antioxidant in blood, can reduce the titer of antibodies in hypercholesterolemia (Table 2.2.4). 

Kontush, A., Spranger, T., Reich, A., Baum, K., and Beisiegel, U., Lipophilic antioxidants in blood plasma as markers of atherosclerosis The role of a-carotene and y-tocopherol. Atherosclerosis, 144, 117-122, 1999. 

Combs, 1992). Ascorbate is also the predominant antioxidant in blood and interstitial fluids (Frei et aL, 1989). 

In addition to ascorbic acid, uric acid is an important antioxidant in blood plasma (9). To assess the antioxidative capacity of plasma it is useful to determine ascorbic acid and uric acid in a single chromatographic run. Ascorbic acid and uric acid have been measured simultaneously from heparinized plasma by UV detection (64). To optimize the detection during method setup, the sample was dissolved in the mobile phase, pH 5.5, where ascorbic acid had the absorbance maximum at 262 nm and uric acid at 285 nm. The wavelength of 262 nm was chosen because ascorbic acid is present at a lower concentration than uric acid in plasma. The same mobile-phase pH (5.5) and UV detection at 280 nm for... 

In summary, the liver has a large reserve capacity and ability to induce antioxidant systems and to excrete Cd complexes luminally into the bile and basola-terally into the circulation. This may account for the lower Cd content of the liver compared to the kidney and explain why Cd toxicity has not been reported in humans. However, it cannot be excluded that subtle alterations of liver function also occur during chronic Cd exposure, which cannot be detected by liver-related biomarkers. Lee and coworkers [249] examined statistical relationships between Cd in urine and circulating antioxidants in blood of humans from the NHANES III database. Circulating levels of a number of these antioxidant markers are primarily controlled by the liver. They found inverse relationships between Cd levels in urine and the levels of circulating antioxidant markers in blood. Thus, these effects may be indirectly linked to the oxidative effects of Cd in the liver and some of these parameters could be useful as Cd biomarkers for liver toxicity in the future. 

BURTON G w, JOYCE A and INGOLD K u (1983) First proof that vitamin E is the major hpid-soluble chain-breaking antioxidant in human blood plasma , Lancet, 2, 327-8. 

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. 

Burton, G., Joyce, A. and Ingold, K.U. (1983). Is vitamin E the only lipid-soluble, chain-breaking antioxidant in human blood plasma and erythrocyte membranes Arch. Biochem. Biophys. 221, 281-290. 

Wayner, D.D., Burton, G.W., Ingold, K.U., Barclay, L.R.C. and Locke, S.J. (1987). Antioxidants in human blood plasma. The relative contributions of vitamin E, urate, ascorbate and protein to the total radical trapping antioxidant activity. Biochim. Biophys. Acta 925, 408-413. 

Sastre, J., Asensi, M., Gasco, E., Pallardo, F.V., Ferrero, J.A., Furukawa, T. and Vina, J. (1992). Exhaustive physical exercise causes oxidation of glutathione status in blood prevention by antioxidant administration. Am. J. Physiol. 263, R992-R995. 

A major contribution of the free-radical scavenging activity in blood plasma is attributable to the macro-molecular proteins (Wayner et al., 1985) of which albumin is a primary component and trapping agertt (Holt et al., 1984). Serum sulphydryl levels, primarily albumin-related, are decreased in subjects with rheumatoid complicated coalworkers pneumoconiosis, indicative of exacerbated inflammatory R.OM production (Thomas and Evans, 1975). Experimental asbestos inhalation in rats leads to an adaptive but evidendy insufficient response by an increase in endogenous antioxidant enzymes (Janssen etal., 1990). Protection of the vascular endothelium against iron-mediated ROM generation and injury is afforded by the iron sequestiant protein ferritin (Balia et al., 1992). 

Figure 10 presents the results of assay of VE and ACL in blood plasma of rabbits treated with probucol and two other synthetic antioxidants (S-l, S-2) for 4 weeks. In addition to an improvement in antioxidative blood plasma protection, in the case of compound S-2 a statistically significant (p < 0.01) decrease in vitamin E content was detected, a finding considered physiologically unfavorable. 

Asai et al. (1999) determined that phospholipid hydroperoxides (PLOOH) are key products for oxidative injury in membranous phospholipid layers in the plasma, red blood cells (RBC), and liver of mice. The formation and accumulation of PLOOH have been confirmed in several cellular disorders, various diseases, and in aging. A lower PLOOH level was found in RBC of the spice-extract-fed mice (65 to 74% of the nonsupplemented control mice). The liver lipid peroxidizability induced with Fe2+/ascorbic acid was effectively suppressed in mice by dietary supplementation with the turmeric and capsicum extracts. Although no difference in the plasma lipids was observed, the liver triacylglycerol concentration of the turmeric-extract-fed mice was markedly reduced to half of the level in the control mice. These findings suggest that these spice extracts could act antioxidatively in vivo by food supplementation, and that the turmeric extract has the ability to prevent the deposition of triacylglycerols in the liver. 

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