In vitro and in vivo effects of selenium and selenium with vitamin E on platelet functions in diabetic rats relationship to platelet sorbitol and fatty acid distribution

1996 ◽  
Vol 55 (3) ◽  
pp. 263-277 ◽  
Author(s):  
Christelle Douillet ◽  
Muriel Bost ◽  
Michèle Accominotti ◽  
Françoise Borson-Chazot ◽  
Maryvonne Ciavatti
Keyword(s):  
Fatty Acid ◽  
Vitamin E ◽  
Fatty Acid Distribution ◽  
Diabetic Rats ◽  
In Vivo Effects ◽  
Platelet Functions

scholarly journals In Vitro and In Vivo Digestibility of Soybean, Fish, and Microalgal Oils, and Their Influences on Fatty Acid Distribution in Tissue Lipid of Mice

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5357
Author(s):  
Bo-Ram Na ◽  
Jeung-Hee Lee
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Distribution ◽  
Docosapentaenoic Acid ◽  
In Vitro Digestion ◽  
Fish Oils ◽  
Microalgal Oil ◽  
Mouse Tissues

The digestion rates of microalgal (docosahexaenoic acid, DHA, 56.8%; palmitic acid, 22.4%), fish (DHA, 10.8%; eicosapentaenoic acid, EPA, 16.2%), and soybean oils (oleic, 21.7%; linoleic acid, 54.6%) were compared by coupling the in vitro multi-step and in vivo apparent digestion models using mice. The in vitro digestion rate estimated based on the released free fatty acids content was remarkably higher in soybean and fish oils than in microalgal oil in 30 min; however, microalgal and fish oils had similar digestion rates at longer digestion. The in vivo digestibility of microalgal oil (91.49%) was lower than those of soybean (96.50%) and fish oils (96.99%). Among the constituent fatty acids of the diet oils, docosapentaenoic acid (DPA) exhibited the highest digestibility, followed by EPA, DHA, palmitoleic, oleic, palmitic, and stearic acid, demonstrating increased digestibility with reduced chain length and increased unsaturation degree of fatty acid. The diet oils affected the deposition of fatty acids in mouse tissues, and DHA concentrations were high in epididymal fat, liver, and brain of mice fed microalgal oil. In the present study, microalgal oil showed lower in vitro and in vivo digestibility, despite adequate DHA incorporation into major mouse organs, such as the brain and liver.

Tocopherol Fate in Plasma and Liver of Streptozotocin-Treated Rats that Orally Received Antioxidants and Spirulina Extracts

2007 ◽  
Vol 77 (4) ◽  
pp. 263-271 ◽  
Author(s):  
García-Martínez ◽  
Rupérez ◽  
Ugarte ◽  
Barbas
Keyword(s):  
Antioxidant Activity ◽  
Vitamin E ◽  
Storage Conditions ◽  
Tocopherol Content ◽  
Diabetic Rats ◽  
Tocopherol Concentration ◽  
Analytical Methodology ◽  
Before And After

Streptozotocin-induced diabetic rats constitute a model of oxidative stress, and vitamin E continues to be a topic of speculation in this area. On the other hand, marine extracts, particularly microalgae extracts obtained with environmentally clean technologies and which demonstrate antioxidant activity in vitro, are a potential source of in vivo antioxidant defense. We have studied the α-tocopherol content in the plasma and liver of diabetic rats after 7 and 14 days under the condition, and before and after the treatment with vitamin E and C, as well as with different Spirulina extracts, as compared with the corresponding controls. The improvement of analytical methodology related to the determination of α-tocopherol in the plasma and liver of rats was also considered. To do this, a method previously developed for plasma, employing a single extraction step, was adapted and validated for liver after minor modifications. Moreover, stability of α-tocopherol in plasma of diabetic and control animals was compared in different storage conditions. Results showed that diabetic plasma strongly influences stability of α-tocopherol, even at –20° C, but samples are stable for at least one year at –80° C. Finally, regarding supplementation, results indicate that supplementation with α-tocopherol increases stored α-tocopherol in liver, but not in plasma, but this availability is strongly dependent on the stage of diabetes of the animal. Extracts of Spirulina platensis, despite showing antioxidant activity in vitro, increased α-tocopherol concentration in neither plasma nor liver.

In vitro antioxidant potential and in vivo effects of Schinus terebinthifolia Raddi leaf extract in diabetic rats and determination of chemical composition by HPLC-ESI-MS/MS

2018 ◽  
Vol 33 (11) ◽  
pp. 1655-1658 ◽  
Author(s):  
Camila Cristina Iwanaga ◽  
Lilian dos Anjos Oliveira Ferreira ◽  
Karine Zanoli Bernuci ◽  
Carla Maria Mariano Fernandez ◽  
Fabiana Brusco Lorenzetti ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Leaf Extract ◽  
Diabetic Rats ◽  
Antioxidant Potential ◽  
Esi Ms ◽  
In Vivo Effects

Effects of Nutritional, Endocrine and Metabolic State on the Development of Intravascular Coagulation Induced by Human Serum Preparations with Procoagulant Activity

1973 ◽  
Vol 29 (01) ◽  
pp. 033-049 ◽  
Author(s):  
Harry N. Antoniades ◽  
Panayotis G. Iatridis ◽  
Nelson Westmoreland ◽  
James D. Simon ◽  
Kenneth C. Hayes ◽  
...  
Keyword(s):  
Human Serum ◽  
Blood Platelet ◽  
Diabetic Rats ◽  
Procoagulant Activity ◽  
Metabolic State ◽  
Intravascular Coagulation ◽  
Serum Fractions ◽  
In Vivo Effects

SummaryInjection of human serum fractions with procoagulant activity into intact rats initiated hypercoagulability, thrombosis and hemorrhage. These in vivo effects were dependent upon the nutritional, endocrine and metabolic state of the animals. Injection in fed rats produced only transient hypercoagulability. In rats fasted 48 hours, the initial hypercoagulability was followed by prolonged hypocoagulation, a decline in blood platelet count, thrombosis and hemorrhage. These effects were reversed in fasted rats by glucose injected 1 hour before the serum fractions. Alloxan-diabetic fed rats and genetically obese fed rats also exhibited enhanced susceptibility to intravascular coagulation on injection of the serum fraction. However, injection of insulin in the diabetic rats before the serum fractions greatly reduced the susceptibility of these animals. The serum fractions used in these studies exhibited potent factor XIIa-like activity in vitro. The present studies demonstrate that the in vivo clotting process can be greatly influenced by the nutritional, endocrine, and metabolic state of the animal and they provide a basis for the investigation of the factors involved.

scholarly journals Effects of a natural PTP1B inhibitor from Rhodomela confervoides on the amelioration of fatty acid-induced insulin resistance in hepatocytes and hyperglycaemia in STZ-induced diabetic rats

RSC Advances ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 3429-3437 ◽  
Author(s):  
Shuju Guo ◽  
Lijun Wang ◽  
Dong Chen ◽  
Bo Jiang
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Diabetic Rats ◽  
Rhodomela Confervoides

A natural bromophenol BPN was identified as a competitive PTP1B inhibitor both in vitro and in vivo.

scholarly journals The influence of vitamin E quinone on platelet structure, function, and biochemistry

Blood ◽  
1980 ◽  
Vol 55 (6) ◽  
pp. 907-914
Author(s):  
AC Cox ◽  
GH Rao ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Vitamin E ◽  
Platelet Function ◽  
Calcium Release ◽  
Adenine Nucleotides ◽  
Antithrombotic Agent ◽  
In Vivo Effects ◽  
Natural Metabolite

Although the effects of vitamin E on platelet function have been investigated in vivo and in vitro, vitamin E quinone, a natural metabolite of vitamin E, has been virtually overlooked. This oxidized form of vitamin E inhibits platelet aggregation and secretion induced by various aggregating agents more effectively than vitamin E by a magnitude of 5–10-fold. Vitamin E and vitamin E quinone do not alter platelet ultrastructure or cellular concentrations of serotonin and adenine nucleotides, including cAMP. Inhibition of aggregation by vitamin E quinone occurs in the absence of detectable reduction of vitamin E quinone or oxidation of vitamin E and is readily reversed by washing the platelet. Only vitamin E quinone prevents arachidonic acid release and slightly inhibits cyclooxygenase, whereas both agents partially prevent calcium release from a platelet subcellular organelle. Vitamin E quinone also inhibited synthesis of prostacyclin by endothelial cells with basal synthesis in the presence of external arachidonic acid being less affected than thrombin-stimulated PGI2 production. The greater potency of vitamin E quinone in suppressing platelet function compared to vitamin E suggests that this quinone metabolite may be the better antithrombotic agent and possibly responsible for in vivo effects previously attributed to vitamin E.

scholarly journals The influence of vitamin E quinone on platelet structure, function, and biochemistry

Blood ◽  
1980 ◽  
Vol 55 (6) ◽  
pp. 907-914 ◽  
Author(s):  
AC Cox ◽  
GH Rao ◽  
JM Gerrard ◽  
JG White
Keyword(s):  
Arachidonic Acid ◽  
Vitamin E ◽  
Platelet Function ◽  
Calcium Release ◽  
Adenine Nucleotides ◽  
Antithrombotic Agent ◽  
In Vivo Effects ◽  
Natural Metabolite

Abstract Although the effects of vitamin E on platelet function have been investigated in vivo and in vitro, vitamin E quinone, a natural metabolite of vitamin E, has been virtually overlooked. This oxidized form of vitamin E inhibits platelet aggregation and secretion induced by various aggregating agents more effectively than vitamin E by a magnitude of 5–10-fold. Vitamin E and vitamin E quinone do not alter platelet ultrastructure or cellular concentrations of serotonin and adenine nucleotides, including cAMP. Inhibition of aggregation by vitamin E quinone occurs in the absence of detectable reduction of vitamin E quinone or oxidation of vitamin E and is readily reversed by washing the platelet. Only vitamin E quinone prevents arachidonic acid release and slightly inhibits cyclooxygenase, whereas both agents partially prevent calcium release from a platelet subcellular organelle. Vitamin E quinone also inhibited synthesis of prostacyclin by endothelial cells with basal synthesis in the presence of external arachidonic acid being less affected than thrombin-stimulated PGI2 production. The greater potency of vitamin E quinone in suppressing platelet function compared to vitamin E suggests that this quinone metabolite may be the better antithrombotic agent and possibly responsible for in vivo effects previously attributed to vitamin E.

In Vitro Incorporation and Metabolism of Icosapentaenoic and Docosahexaenoic Acids in Human Platelets - Effect on Aggregation

1986 ◽  
Vol 56 (01) ◽  
pp. 057-062 ◽  
Author(s):  
Martine Croset ◽  
M Lagarde
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Platelet Aggregation ◽  
Fatty Acid Distribution ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Aggregation Response ◽  
Docosahexaenoic Acids ◽  
Membrane Level

SummaryWashed human platelets were pre-loaded with icosapentaenoic acid (EPA), docosahexaenoic acid (DHA) or EPA + DHA and tested for their aggregation response in comparison with control platelets. In fatty acid-rich platelets, an inhibition of the aggregation could be observed when induced by thrombin, collagen or U-46619. The strongest inhibition was observed with DHA-rich platelets and it was reduced when DHA was incorporated in the presence of EPA.Study of fatty acid distribution in cell lipids after loading showed that around 90% of EPA or DHA taken up was acylated into phospholipids and a very small amount (less than 2%) remained in their free and hydroxylated forms. DHA was more efficiently acylated into phosphatidylethanolamine (PE) than into phosphatidylinositol (PI) in contrast to what observed with EPA, and both acids were preferentially incorporated into phosphatidylcholine (PC). EPA inhibited total incorporation of DHA and increased its relative acylation into PE at the expense of PC. In contrast, DHA did not affect the acylation of EPA. Upon stimulation with, thrombin, EPA was liberated from phospholipids and oxygenated (as judged by the formation of its monohydroxy derivative) whereas DHA was much less metabolized, although consistently transferred into PE.It is concluded that EPA and DHA might affect platelet aggregation via different mechanisms when pre-loaded in phospholipids. Whereas EPA is known to alter thromboxane A2 metabolism from endogenous arachidonic acid, by competing with it, DHA might act directly at the membrane level for inhibiting aggregation.

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