scholarly journals The synergistic effect of daidzein and α-tocopherol or ascorbic acid on microsome and LDL oxidation

2010 ◽  
Vol 28 (No. 5) ◽  
pp. 385-391 ◽  
Author(s):  
H. Wang ◽  
M.W. Martin ◽  
S. Yin
Keyword(s):  
Ascorbic Acid ◽  
Antioxidant Properties ◽  
Liver Microsomes ◽  
Oxidative Modification ◽  
Alpha Tocopherol ◽  
Interactive Effects ◽  
Ldl Oxidation ◽  
Rat Liver Microsomes ◽  
Protective Effects ◽  
Potential Health

Isoflavone daidzein brings potential health benefits. Its antioxidant properties are considered to be responsible in part for its protective effects. We investigated the antioxidant effects of daidzein and its interactive effects with<br />&alpha;-tocopherol or ascorbic acid on Fe<sup>2+/</sup>ascorbate-induced oxidation of rat liver microsomes and copper-induced human low-density lipoprotein (LDL) oxidation. Although the inhibitory effect of daidzein on lipid peroxidation in microsome was weak, it effectively prevented LDL against oxidative modification by prolonging the lag time, decreasing the propagating rate, and suppressing malonaldehyde (MDA) and carbonyls formation. When daidzein was combined with &alpha;-tocopherol in microsomes oxidation and with ascorbic acid in LDL oxidation, the protection was significantly greater than the calculated additive effect of the two individual actions. Thus, daidzein can protect LDL from oxidative modification, and its combination with nutrients may be superior to the action of it alone. These results can help to get a better understanding of the interactions of different antioxidants in vivo.

Vitamin E, Atherosclerosis and Thrombosis

2001 ◽  
Vol 85 (05) ◽  
pp. 766-770 ◽  
Author(s):  
Fausta Micheletta ◽  
Luigi Iuliano ◽  
Francesco Violi
Keyword(s):  
Biological Activity ◽  
Vitamin E ◽  
Daily Intake ◽  
Atherosclerotic Lesion ◽  
Redox Status ◽  
Oxidative Modification ◽  
Alpha Tocopherol ◽  
Ldl Oxidation ◽  
Alternative Mechanism ◽  
Chain Breaking

SummaryVitamin E, a major lipid-soluble, chain-breaking antioxidant includes several tocopherols having the biological activity of RRR-alpha-tocopherol. Vitamin E circulates in the blood as free tocopherol bound to beta-lipoproteins and is present in cell membrane where it exerts a potent defence against lipid peroxidation (1). Blood concentration of vitamin E in humans ranges from 25 to 30 μM, depending on daily intake and body’s ability to absorb fat (1). In the last decade the scientific interest on biological activity of vitamin E increased because of a growing body of evidence linking this vitamin with atherosclerosis and its complications (2). Thus, the oxidative hypothesis of atherosclerosis suggests that LDL accumulates within vessel wall, in particular in the macrophages, as a consequence of its oxidative modification mediated by resident cells (3, 4). A reduced defence against LDL oxidation could favour this process and accelerate atherosclerotic progression. Accordingly, patients with coronary heart disease have lower plasma concentration of vitamin E than controls (2) and prospective studies demonstrated that a daily assumption of vitamin E reduces cardiovascular events (5). According to the oxidative hypothesis of atherosclerosis, this effect has been attributed to the inhibition of LDL oxidation. Alternative mechanism potentially implicated in the antiatherosclerotic activity of vitamin E includes its interference with the activity of platelet and monocyte, in which the intracellular redox status plays an important functional role (6, 7). As platelets and monocytes are both involved in the pathophysiologic process leading to atherosclerotic lesion, the interference of vitamin E with the biological function of these cells may represent another important tool to explore the anti-atherosclerotic activity of vitamin E. This review will focus on the open issues related to the use of vitamin E in clinical studies and the potential usefulness in investigating platelet function and clotting activation in patients treated with vitamin E.

scholarly journals In vitro antioxidant activity of meniran (Phyllantus urinaria) functional drink in human low density lipoprotein (LDL)

2021 ◽  
Vol 913 (1) ◽  
pp. 012093
Author(s):  
U Fitrotin ◽  
N Hilmiati ◽  
Mardiana ◽  
Y Triguna ◽  
A Surahman ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Phenolic Content ◽  
Radical Scavenging Activity ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Functional Drink

Abstract Preparation process for meniran (Phillantus urinaria) functional drink (MFD) influences its antioxidant activity. This research aims to understand the phenolic content, DPPH Radical Scavenging Activity (RSA), and LDL oxidation of MFD through various preparation processes. Those preparation processes included soaking fresh meniran (SFM), boiling fresh meniran for 5 minutes (BFM5’), boiling fresh meniran for 10 minutes (BFM10’), and soaking dried meniran (DM). The phenolic content was determined with Folin–Ciocalteu, antioxidant activity was assessed using DPPH and TBARS assay with LDL as the oxidation substrate. An antioxidant references in this research used ascorbic acid. The phenolic content in methods of SFM, BFM5’, BFM10’ and DM were 122±0.022, 182±0.043, 192 ±0.03, and 117 ±0.019 mg GAE/g of meniran respectively. Meanwhile, the DPPH RSA of SFM, BFM5’, BFM10’ and DM accounted for 82.18±0.35, 86.19±0.53, 86.75±0.64 and 69.96% respectively. As comparison, the DPPH RSA of ascorbic acid 50 ppm is 75.65±0.82%. At the same time the optimum inhibition of TBARS formation from BFM5’ and BFM10’ methods were 45.83 % and 48.66%, with MDA concentration in human LDL accounted for 38.30±2.39 and 36.30±1.82 nmol MDA/mg protein, respectively. As comparison, MDA concentration in human LDL added with ascorbic acid 25 ppm accounted for 41.35±2.41 nmol MDA/mg protein. In contrast, the control human LDL was 70.70±2.35 nmol MDA/mg protein. This study concludes that the BFM5’ and BFM10’ methods showed the highest antioxidant properties compared to other methods. All methods showed that MFD extract in concentration more than 25 ppm increased the concentration of MDA in human LDL. Therefore, to produce meniran functional drink in optimum antioxidant properties is best by using BFM5’ and BFM10’ preparation methods in meniran concentration of not more than 25 ppm.

scholarly journals Effects of vitamins A and D on the biosynthesis of l-ascorbic acid by rat-liver microsomes

1965 ◽  
Vol 97 (1) ◽  
pp. 247-249 ◽  
Author(s):  
NC Ghosh ◽  
I Chatterjee ◽  
GC Chatterjee
Keyword(s):  
Vitamin D ◽  
Ascorbic Acid ◽  
Vitamin A ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Stock Diet ◽  
Hypervitaminosis A ◽  
Hypervitaminosis D ◽  
Liver Tissues

1. The synthesis of l-ascorbic acid from either d-glucuronolactone or l-gulonolactone by liver microsomes of rats is decreased under conditions of hypervitaminosis A; under hypervitaminosis D the synthesis from d-glucuronolactone is increased and that from l-gulonolactone is not affected. 2. The microsomal conversion of l-gulonolactone into l-ascorbic acid is impaired in liver tissues of rats made deficient with respect to either vitamin A or vitamin D when compared with the controls maintained on stock diet.

scholarly journals The mechanism of initiation of lipid peroxidation. Evidence against a requirement for an iron(II)-iron(III) complex

1989 ◽  
Vol 258 (2) ◽  
pp. 617-620 ◽  
Author(s):  
O I Aruoma ◽  
B Halliwell ◽  
M J Laughton ◽  
G J Quinlan ◽  
J M C Gutteridge
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Brain Phospholipids ◽  
Lag Period

When Fe2+ ions are added to rat-liver microsomes, lipid peroxidation begins after a short lag period. Fe2+-dependent peroxidation in the first few minutes of the incubation can be increased by adding Fe3+, ascorbic acid or Pb2+ ions; these stimulations are not additive. By contrast, Pb2+ ions inhibit peroxidation of microsomes in the presence of Fe3+/ascorbate or Fe3+-ADP/NADPH. In liposomes made from ox-brain phospholipids, Fe2+-dependent peroxidation is stimulated slightly by Fe3+, but much more so by ascorbic acid, Al3+ or Pb2+; these stimulations are not additive. Liposomal peroxidation in the presence of Fe3+/ascorbate is inhibited by Pb2+ or Al3+. These results argue against the participation of an Fe2+-Fe3+-O2 complex, or a critical 1:1 ratio of Fe2+ to Fe3+, in the initiation of lipid peroxidation in liposomes and rat-liver microsomes.

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