The Influence of Ascorbic Acid on Platelet Structure and Function

1975 ◽  
Vol 34 (01) ◽  
pp. 050-062
Author(s):  
Dale H Cowan ◽  
Richard C Graham ◽  
Patricia Shook ◽  
Ronda Griffin
Keyword(s):  
Ascorbic Acid ◽  
Open Channel ◽  
Channel System ◽  
Short Intervals ◽  
Platelet Survival ◽  
Artifactual Changes ◽  
Survival Studies ◽  
And Function ◽  
Induced Aggregation ◽  
Platelet Structure

SummaryTo determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidifìcation levels. The effect of ascorbic acid (A. A.) was compared to that of HCl and citric acid (C. A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A. A. and C. A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultra-structure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A. A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

Platelet Survival and Function in Animals with Prosthetic Mitral Valve: The Effect of Nafazatrom

1984 ◽  
Vol 52 (02) ◽  
pp. 099-101
Author(s):  
H Al-Mondhiry ◽  
W S Pierce ◽  
W Richenbacher
Keyword(s):  
Platelet Aggregation ◽  
Heart Valves ◽  
Ex Vivo ◽  
Oral Drug ◽  
Prosthetic Heart Valves ◽  
Antithrombotic Agent ◽  
Mitral Valves ◽  
Platelet Survival ◽  
Survival Studies ◽  
And Function

SummaryThromboembolism remains a serious problem in patients with prosthetic heart valves. Previous studies documented a number of platelet abnormalities in such patients and correlated the occurrence of thromboembolic complications with short platelet survival. We have studied platelet survival and platelet aggregation in eight goats fitted with prosthetic mitral valves and repeated the studies following treatment with nafazatrom, a potent antithrombotic agent. Eleven survival studies in eight animals showed a platelet survival not significantly different from control (6.52 ± 0.72 vs. 6.94 ± 0.81 days). Following seven to ten days of oral drug administration, platelet survival in the test animals was 7.34 ± 0.96 days, significantly longer than pretreatment results (p <0.01). Animals with the shortest pretreatment platelet survival achieved substantial prolongation of platelet life span following drug treatment. The drug caused no change in ex vivo platelet aggregation.

Influence of Ascorbic Acid on the Structure and Function of Alpha-2- macroglobulin: Investigations using Spectroscopic and Thermodynamic Techniques

2020 ◽  
Vol 27 (3) ◽  
pp. 201-209
Author(s):  
Syed Saqib Ali ◽  
Mohammad Khalid Zia ◽  
Tooba Siddiqui ◽  
Haseeb Ahsan ◽  
Fahim Halim Khan
Keyword(s):  
Ascorbic Acid ◽  
Conformational Changes ◽  
Structural Changes ◽  
The Body ◽  
Titration Calorimetry ◽  
Spectroscopic Techniques ◽  
Human Beings ◽  
Plasma Ascorbic Acid ◽  
Dietary Antioxidant ◽  
And Function

Background: Ascorbic acid is a classic dietary antioxidant which plays an important role in the body of human beings. It is commonly found in various foods as well as taken as dietary supplement. Objective: The plasma ascorbic acid concentration may range from low, as in chronic or acute oxidative stress to high if delivered intravenously during cancer treatment. Sheep alpha-2- macroglobulin (α2M), a human α2M homologue is a large tetrameric glycoprotein of 630 kDa with antiproteinase activity, found in sheep’s blood. Methods: In the present study, the interaction of ascorbic acid with alpha-2-macroglobulin was explored in the presence of visible light by utilizing various spectroscopic techniques and isothermal titration calorimetry (ITC). Results: UV-vis and fluorescence spectroscopy suggests the formation of a complex between ascorbic acid and α2M apparent by increased absorbance and decreased fluorescence. Secondary structural changes in the α2M were investigated by CD and FT-IR spectroscopy. Our findings suggest the induction of subtle conformational changes in α2M induced by ascorbic acid. Thermodynamics signatures of ascorbic acid and α2M interaction indicate that the binding is an enthalpy-driven process. Conclusion: It is possible that ascorbic acid binds and compromises antiproteinase activity of α2M by inducing changes in the secondary structure of the protein.

Decreased Platelet Vitamin C in Diabetes Mellitus; Possible Role in Peraggregatoon

1979 ◽  
Author(s):  
K.E. Sarji ◽  
J. Gonzalez ◽  
H. Hempling ◽  
J.A. Colwell
Keyword(s):  
Ascorbic Acid ◽  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Vitamin C ◽  
Platelet Rich Plasma ◽  
Solution Ph ◽  
Dose Dependent Fashion ◽  
Insulin Dependent Diabetic ◽  
Induced Aggregation

To determine whether Vitamin C might relate to the increased platelet sensitivity in the diabetic, we have measured levels of platelet Vitamin C and studied the effects of Vitamin C on platelet aggregation. Ascorbic acid levels in washed platelets from diabetics were significantly lower than from normals (4s.2±3 μg/1010 platelets vs. 2s.s±2 μg/1010 platelets, p<.001). The effects of ascorbic acid on platelet aggregation in vitro were studied by adding ascorbic acid in buffered solution (pH 7.35) prior to-aggregating agents. Ascorbic acid in platelet-rich plasma consistently inhibited platelet aggregation with threshold concentrations of ADP, epinephrine, and collagen. With washed platelets, ascorbic acid inhibited arachidonic, acid-induced aggregation. When platelets were incubated at 37°C for 10 minutes with varying concentrations of ascorbic acid, rewashed, and aggregation with arachidonic acid tested, aggregation was inhibited in a linear dose-dependent fashion. Oral ingestion of ascorbic acid (2 gm/day) for seven days by normal non-smoking males produced a marked inhibition of aggregation. In a similar study, platelets from an insulin-dependent diabetic showed no change in aggregation. These results suggest that platelet levels of ascorbic acid may relate to the hyperaggregat ion of platelets from diabetics.

scholarly journals Ultrastructural Study of Platelet Aggregation by Mouse 15091A Tumor Cells

1977 ◽  
Author(s):  
G.J. Stewart ◽  
R.A. Kuprionas ◽  
G.J. Gasic ◽  
J. Catalfamo ◽  
G.P. Gasic
Keyword(s):  
Platelet Aggregation ◽  
Tumor Cells ◽  
Lysosomal Enzymes ◽  
Culture Medium ◽  
Open Channel ◽  
Channel System ◽  
Transmission Electron ◽  
Spherical Vesicles ◽  
Aggregation Of Platelets ◽  
Soluble Material

Most tumor cells cause aggregation of platelets in heparinized plasma via material shed into culture medium. In this study we investigated the events by transmission electron microscopy. Freshly washed cells were covered with closely spaced microvilli, many of which pinched off during 1 hour of incubation at 37°C. Both cells and shed microvilli were membrane enclosed. Shed microvilli became spherical vesicles containing cytoplasm. Platelets aggregated when stirred with incubated tumor cells or shed material. The aggregates were composed of platelets that showed pseudopod formation, centralization of granules and increase in the open channel system. Platelets around the periphery of aggregates had bulbous portions free of granules (ballooning) but many granules remained in platelets in the interior of aggregates suggesting that release of lysosomal enzymes may have been somewhat limited. Aggregates resembled those induced by ADP rather than by thrombin. Tumor cells were not incorporated into the aggregates. Vesicles were not selectively associated with platelets prior to or during aggregation. While some vesicles were incorporated into aggregates, it appeared that this was a consequence rather than the cause of aggregation. Therefore, vesicles may have produced soluble material that induced platelet aggregation.

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