scholarly journals Mechanisms of Ascorbyl Radical Formation in Human Platelet-Rich Plasma

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Kou-Gi Shyu ◽  
Chao-Chien Chang ◽  
Yu-Chieh Yeh ◽  
Joen-Rong Sheu ◽  
Duen-Suey Chou
Keyword(s):  
Free Radical ◽  
Enzyme Inhibitors ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Complex Iii ◽  
Free Radical Scavengers ◽  
Doublet Signal ◽  
Spin Resonance ◽  
Generation Mechanisms ◽  
Oxide Synthase

Recently, many clinical reports have suggested that the ascorbyl free radical (Asc∙) can be treated as a noninvasive, reliable, real-time marker of oxidative stress, but its generation mechanisms in human blood have rarely been discussed. In this study, we used upstream substances, enzyme inhibitors, and free radical scavengers to delineate the mechanisms ofAsc∙formation in human platelet-rich plasma (PRP). Our results show that the doublet signal was detected in PRP samples by using electron spin resonance, and the hyperfine splitting of the doublet signal wasaH=1.88gauss andg-factor = 2.00627, which was determined to be theAsc∙. We observed that the inhibitors of NADPH oxidase (NOX), cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP450), mitochondria complex III, and nitric oxide synthase (NOS), but not xanthine oxidase, diminished the intensity of theAsc∙signal dose dependently. All enzyme inhibitors showed no obvious antioxidant activity during a Fenton reaction assay. In summary, the obtained data suggest thatAsc∙formation is associated with NOX, COX, LOX, CYP450, eNOS, and mitochondria in human PRP.

Novel C-9, 9'-O-acyl Esters of (-)-Carinol as Free-radical Scavengers and Xanthine Oxidase Enzyme Inhibitors: Synthesis and Biological Evaluation

2013 ◽  
Vol 9 (1) ◽  
pp. 100-103 ◽  
Author(s):  
Praveen Kumar Suryadevara ◽  
Hari Babu Tatipaka ◽  
Rama Subba Rao Vidadala ◽  
Ashok k Tiwari ◽  
Janaswamy Madhusudana Rao ◽  
...  
Keyword(s):  
Free Radical ◽  
Xanthine Oxidase ◽  
Enzyme Inhibitors ◽  
Biological Evaluation ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxidase Enzyme ◽  
Synthesis And Biological Evaluation

Novel C-9, 9'-O-acyl Esters of (-)-Carinol as Free-radical Scavengers and Xanthine Oxidase Enzyme Inhibitors: Synthesis and Biological Evaluation

2012 ◽  
Vol 9 (1) ◽  
pp. 100-103
Author(s):  
Praveen Kumar Suryadevara ◽  
Hari Babu Tatipaka ◽  
Rama Subba Rao Vidadala ◽  
Ashok k Tiwari ◽  
Janaswamy Madhusudana Rao ◽  
...  
Keyword(s):  
Free Radical ◽  
Xanthine Oxidase ◽  
Enzyme Inhibitors ◽  
Biological Evaluation ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxidase Enzyme ◽  
Synthesis And Biological Evaluation

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

1988 ◽  
Vol 59 (02) ◽  
pp. 236-239 ◽  
Author(s):  
Giovanna Barzaghi ◽  
Chiara Cerletti ◽  
Giovanni de Gaetano
Keyword(s):  
Platelet Aggregation ◽  
Receptor Antagonist ◽  
Phospholipase C ◽  
Clostridium Perfringens ◽  
Human Platelet ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
Platelet Activating Factor ◽  
Inhibitory Effect ◽  
Thromboxane Receptor Antagonist

SummaryWe studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37° C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAG) of PLC was 3-4 U/ml.We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshold concentrations. We also studied the possible inhibitory effect of aspirin, apyrase, TMQ, a prostaglandin endoper- oxide/thromboxane receptor antagonist and BN-52021, a PAF receptor antagonist. Only aspirin and apyrase were able to reduce aggregation induced by PLC alone and PLC + AA and PLC + ADP respectively. TMQ and BN-52021 were inactive. In ex vivo experiments oral aspirin (500 mg) partially inhibited platelet aggregation induced by PLC alone, PLC + AA and PLC + ADP 2 and 24 h after administration. Aspirin 20 mg for 7 days also reduced aggregation induced by PLC + AA.

Inhibitory Effect of Staphylokinase on Platelet Aggregation

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Degradation Products ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Effective Concentration ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Washed Platelet ◽  
Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

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