Lipoproteins periodate oxidation

Limited studies have focused on dietary intake of astaxanthin by humans. In a study reported by Miki, an astaxanthin-containing drink was used to protect low-density lipoprotein from oxidation (astaxanthin was administered at doses of 3.6 to 14.4 mg/day over a 2-week period). Progressive slowing of LDL oxidation with increasing doses of astaxanthin was observed and no ill effects were reported. 

The effects of wine and its polyphenol constituents on early indicators of coronary heart disease such as elevated levels of plasma lipids, platelets and serum antioxidant activity were discussed in a review by Cooper et al. (2004). This review also addressed whether the polyphenols or alcohol are responsible for the beneficial effects of wine on cardio-vascular health. The authors conclude that red wine polyphenols have little effect on plasma lipid concentrations, but that wine consumption reduces the susceptibility of low-density lipoprotein (LDL) cholesterol to oxidation and increase serum antioxidant capacity. These effects, however, do depend on the amount of wine that is consumed and the period of supplementation. It was suggested that specific polyphenols appear to have endothelium-dependent vaso-relaxing abilities. Red wine phenolics also have an inhibitory effect on platelet aggregation. Evidence suggests that alcohol has a positive synergistic effect with wine polyphenols on some atherosclerosis risk factors. Thus, evidence that wine drinking is beneficial for cardiac health appears positive. 

Within the developing embryo, lipoprotein lipase activity is high in both heart and adipose tissue at EI4 but is absent from liver and brain. A big increase in activity occurs in adipose tissue between EI2 and EI6 and this coincides with the period of lipid uptake from the yolk and deposition in the adipocytes. More than 90% of the energy required by the developing embryo is obtained from oxidation of fatty acids present in yolk triglycerides. A further increase in lipoprotein lipase activity also occurs on hatching (Speake, Noble McCartney, 1993). 

There is a growing body of evidence suggesting that oxidation of low density lipoprotein (LDL)-cholesterol particles may be a pivotal step in atherogenesis (28-30). Cigaret smoking, even for brief periods, can markedly enhance LDL-cholesterol oxidation as well as decrease high-density lipoprotein cholesterol (31). It also depletes body stores of vitamin C that may be an important antioxidant protection. Intake of the anti-oxidant beta carotene has been shown to be inversely related to the risk of coronary events among current smokers (relative risk 0.30) and former smokers (relative risk 0.60), but was not beneficial in persons who had never smoked (32,33). 

Figure 6 Pomegranate juice consumption by E° mice reduces macrophage-mediated LDL oxidation mechanisms. Mouse peritoneal macrophages (MPMs) were isolated from the peritoneal fluid of control E° mice or from mice that consumed 12.5 i.iL of pomegranate juice (PJ)/mouse/day, for a period of 2 months. (A) Cell-mediated LDL oxidation. The MPMs were incubated for 6 h at 37 °C with LDL (100 pg protein/mL) under oxidative stress (in the presence of 2 pM of CUSO4). LDL oxidation was measured directly in the medium by the TEARS assay. Results are expressed as mean + S.D. (n = 3). p < 0.01 (vs. placebo). (B) MPM lipid peroxidation was determined as cellular lipid peroxides. (C) Superoxide anion release The amount of superoxide anion release from the MPM to the medium in response to 50 ng/mL of PMA was determined. (D) Total glutathione was determined in MPM sonicate supernatant with the 5,5-dithiobis-2-nitrobenzoic acid-glutathione reductase (NADPH) recycling assay. (E) Results are expressed as mean + S.D. n = 3). p < 0.01 (vs. control). LDL, low-density lipoprotein TEARS, thiobarbituric acid reactive substance PMA,...

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