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Lipid delaying effect

The crystallization behavior of milk fat (which contains minor lipids) and a pure triacylglycerol fraction of milk fat were compared by Herrera et al. (1999). The results suggested that minor lipids delay nucleation but promote crystal growth. Other workers who examined the effects of added phospholipids on palm oil, suggested that some phospholipids delayed nucleation while others had more significant effects on the rate of growth of fat crystals (Smith, 2000),... [Pg.312]

Mercury is unusual in its ability to induce delayed neurological effects. This is especially prevalent with exposure to alkyl mercury compounds. In such cases, the onset of adverse effects may be delayed for months after the initial exposure. The delayed effects of methyl- and dimethylmercury reported in human poisonings are thought, in part, to result from binding to red blood cells, and subsequent slow release. Methylmercury also forms a complex in plasma with the amino acid cysteine, which is structurally similar to the essential amino acid methionine (Aschner and Clarkson 1988). Clarkson (1995) proposed that methylmercury can cross the blood-brain barrier "disguised" as an amino acid via a carrier-mediated system (i.e., transport is not solely the result of methylmercury s lipid solubility). [Pg.248]

Idebenone, an inhibitor of lipid peroxidation, was shown to prolong survival time and delay the onset of ischaemic seizures in a bilateral carotid occlusion model in rats. It is marketed in Japan as a therapy to improve cerebral metabolism and performance after a stroke (Suno and Nagaoka, 1984). Cerebral protective effects after an ischaemic insult in dogs and rabbits have been seen with the hydroxyl radical scavenger, mannitol (Meyer et al., 1987). [Pg.270]

Flavonoids protect LDL from oxidation, delaying the onset of lipid peroxidation, however, the prevention of atherosclerosis by flavonoids occurs not only by the inhibition of LDL oxidation, but also by the increase of cellular resistance to harmful effects of the oxidized LDL (de Luis and Aller, 2008). The antioxidant activity of anthocyanidins, as well as their protective role against LDL oxidation, has been well demonstrated in different in vitro systems (Aviram and Fuhrman, 2002 Satue-Gracia and others 1997 Teissedre and others 1996). [Pg.160]

Replacement of the famesyl group by lipid analogues could be performed for full length Ras proteins in vitro by means of the enzyme famesyltrans-ferase. When such partially modified Ras constructs were applied in Xenopus oocytes the cellular machinery completed modification (endoprotease activity, carboxymethylation and palmitoylation). In these cases the H-Ras famesyl group could be stripped off most of its isoprenoid features that distinguish it from a fatty add without any apparent effect on its ability to induce oocyte maturation and activation of mitogen-activated protdn kinase In contrast, replacement by the less hydrophobic isoprenoid geranyl causes severely delayed oocyte activation. [Pg.379]

Pheromone (sex attractant). Ether extract of the stem, produced equivocal effect on Aspiculuris tetraptera, female and male Dacus dorsalis, male Mediterranean fruit flies, and male and female melon flies " k Pheromone (signaling). Ether extract of the stem, produced equivocal effect on Aspiculuris tetraptera, female and male Dacus dorsalis, male Mediterranean fruit flies, and male and female melon flies " k Phospholipidemic effect. Oil, administered to phospholipids transfer protein knockout (PLTPO)-deficient mice, produced an increase of phospholipids and free cholesterol in the VLDL-LDL region of PLTPO mice. Accumulation of phospholipids and free cholesterol was dramatically increased in PLTPO/HLO mice compared to PLTPO mice. Turnover studies indicated that coconut oil was associated with delayed catabolism of phospholipids and phospho-lipids/free cholesterol-rich particles. Incubation of these particles with hepatocytes of coconut-fed mice produced a reduced removal of phospholipids and free cholesterol by SRBI, even though SRBI protein expression levels were unchanged . [Pg.139]

At 600 ng/kg BW, no adverse effects on survival, growth, or reproduction. At 1200 ng/kg BW, spawning was delayed 13 days. Dietary assimilation of 2,3,7,8-TCDD is high at 89% and is independent of time and whole-body TCDD burdens. Regardless of dose, ovarian tissues of adult females had 74% of the whole-body 2,3,7,8-TCDD concentration on a lipid weight basis and 61% on a nonlipid basis. Spawned eggs had 39% of the whole-body 2,3,7,8-TCDD concentration on a nonlipid basis... [Pg.1048]

Methyinaltrexone is a quaternary derivative of the opioid antagonist, naltrexone. The addition of the methyl group forms a compound with greater polarity and lower lipid solubility, so that it is poorly absorbed, and does not cross the blood-brain barrier. Methyinaltrexone distributes selectively (>200-fold selectivity) to peripheral receptors. In human trials it prevented morphine-induced delay in gastrointestinal transit time, while sparing centrally mediated analgesic effects. [Pg.131]


See other pages where Lipid delaying effect is mentioned: [Pg.388]    [Pg.2868]    [Pg.448]    [Pg.195]    [Pg.89]    [Pg.174]    [Pg.629]    [Pg.79]    [Pg.352]    [Pg.302]    [Pg.225]    [Pg.104]    [Pg.29]    [Pg.408]    [Pg.485]    [Pg.33]    [Pg.189]    [Pg.102]    [Pg.108]    [Pg.139]    [Pg.47]    [Pg.339]    [Pg.331]    [Pg.249]    [Pg.450]    [Pg.391]    [Pg.408]    [Pg.485]    [Pg.47]    [Pg.75]    [Pg.130]    [Pg.552]    [Pg.614]    [Pg.93]    [Pg.125]    [Pg.65]    [Pg.331]    [Pg.576]    [Pg.150]    [Pg.376]    [Pg.242]    [Pg.333]    [Pg.363]   
See also in sourсe #XX -- [ Pg.2868 ]




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