Effects of riboflavin-2',3',4',5'-tetrabutyrate and flavin adenine dinucleotide on the platelet aggregation induced by hydrogen peroxide.

Higashi, Ototaka; Ishigaki, Wakako; Hashimoto, Teiji

doi:10.1620/tjem.124.323

Cited by 7 publications

(4 citation statements)

References 18 publications

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“…The first possibility is that FAD might influence the metabolism of prostaglandin endoperoxides through the glutathione peroxidase and reductase system in the cell, because there are some enzymes which either require glutathione or are stabilized by glutathione (Machlin 1978;Higashi et al 1978; Christ-Hazelhof and Nugteren 1979; Shimizu et al 1979). The second possibility is that FAD might inhibit phospholipase, which liberates arachidonic acid from phospholipid pool in the platelet membrane, when the cell was stimulated by platelet aggregation inducers, such as ADP or collagen (Malmsten et al 1977).…”

Section: Discussionmentioning

confidence: 99%

“…This could be the mechanism of the inhibitory effect of FAD upon the platelet functions. The intravenous drip infusion of FAD in a dose of 0.2 mg/kg within 30 min was followed by no marked decrease of platelet aggregation, probably because the plasma concentration of FAD and/or AMP did not reach the levels high enough to suppress the platelet functions.-------FAD; AMP; platelet aggregation; platelet ATP release; FAD hydrolyzing enzyme activity of blood plasma; 1-14C-arachidonic acid metabolism Previously flavine adenine dinucleotide (FAD) has been shown to have an inhibitory effect on the platelet aggregation in vitro (Clayton et al 1963;Kuzuya 1977;Higashi et al 1978;Shimada et al 1980). Such an inhibitory effect of FAD on the platelet function could be demonstrated not only in vitro but also in vivo, when a large dose of FAD was administered intravenously (Shimada et al 1980).…”

mentioning

confidence: 99%

“…-------FAD; AMP; platelet aggregation; platelet ATP release; FAD hydrolyzing enzyme activity of blood plasma; 1-14C-arachidonic acid metabolism Previously flavine adenine dinucleotide (FAD) has been shown to have an inhibitory effect on the platelet aggregation in vitro (Clayton et al 1963;Kuzuya 1977;Higashi et al 1978;Shimada et al 1980). Such an inhibitory effect of FAD on the platelet function could be demonstrated not only in vitro but also in vivo, when a large dose of FAD was administered intravenously (Shimada et al 1980).…”

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confidence: 99%

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Further studies on the effects of flavine adenine dinucleotide on the platelet functions.

Shimada

Takahashi

Watanabe

et al. 1983

Tohoku J. Exp. Med.

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Flavine adenine dinucleotide (FAD) may inhibit not only the aggregation but also ATP release of platelets in vitro. FAD did not inhibit the synthesis of thromboxane from 1-14C-arachidonic acid by platelets. FAD was found to be hydrolyzed to FMN and AMP by a plasma enzyme, the activity of which in normal adults being estimated as 32.6+9.1 m,uM/ml plasma/min and AMP, thus produced, and/or FAD might compete for the receptor sites on the platelet surface. This could be the mechanism of the inhibitory effect of FAD upon the platelet functions. The intravenous drip infusion of FAD in a dose of 0.2 mg/kg within 30 min was followed by no marked decrease of platelet aggregation, probably because the plasma concentration of FAD and/or AMP did not reach the levels high enough to suppress the platelet functions.-------FAD; AMP; platelet aggregation; platelet ATP release; FAD hydrolyzing enzyme activity of blood plasma; 1-14C-arachidonic acid metabolism Previously flavine adenine dinucleotide (FAD) has been shown to have an inhibitory effect on the platelet aggregation in vitro (Clayton et al. 1963;Kuzuya 1977;Higashi et al. 1978;Shimada et al. 1980). Such an inhibitory effect of FAD on the platelet function could be demonstrated not only in vitro but also in vivo, when a large dose of FAD was administered intravenously (Shimada et al. 1980).The present investigation was conducted to study the effect of FAD upon the adenosine triphosphate (ATP) release of platelets, the mechanism of action of FAD and the in vivo effect of FAD in an ordinary dose upon the platelet functions. MATERIALS AND METHODSBlood was obtained from normal adult volunteers.Methods were similar to those described in the previous paper (Shimada et al. 1980) unless otherwise indicated.The platelet aggregation and ATP release were measured simultaneously by the use of the Lumi-aggregometer (Chrono-Log Corporation, Havortown, Pa). The citrated platelet-rich plasma (PRP) was preincubated with or without FAD of various concentrations for 20 min, and then the aggregating agent, collagen (HormonChemie, Munchen) or arachidonic acid (Silver et al. 1973) was added.For the study of arachidonic acid-induced platelet aggregation, both PRP and washed platelet suspensions in 0.15 M Tris HCl buffer, pH 7.4 (Okuma 1976) were used.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Further studies on the effects of flavine adenine dinucleotide on the platelet functions.

Shimada

Takahashi

Watanabe

et al. 1983

Tohoku J. Exp. Med.

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“…Glutathione peroxidase (GPx) reduces the intracellular H 2 O 2 and toxic fatty acid hydroperoxides to water and in turn, GSH (reduced form) to GSSG (oxidized form). Glutathione reductase (GR), the enzyme that restores intracellular GSH (reduced form) levels by reducing GSSG (oxidized form) in an NADPH-mediated reaction, utilizes FAD as a cofactor (Higashi et al, 1978). Imbalance in the glutathione system has been shown to cause elevated retinal lipid peroxidation (Puertas et al, 1993).…”

Section: Retinal Flavin Homeostasis and Oxidative Balancementioning

confidence: 99%

Flavins Act as a Critical Liaison Between Metabolic Homeostasis and Oxidative Stress in the Retina

Sinha

Naash

Al‐Ubaidi

2020

Front. Cell Dev. Biol.

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Derivatives of the vitamin riboflavin, FAD and FMN, are essential cofactors in a multitude of bio-energetic reactions, indispensable for lipid metabolism and also are requisites in mitigating oxidative stress. Given that a balance between all these processes contributes to the maintenance of retinal homeostasis, effective regulation of riboflavin levels in the retina is paramount. However, various genetic and dietary factors have brought to fore pathological conditions that co-occur with a suboptimal level of flavins in the retina. Our focus in this review is to, comprehensively summarize all the possible metabolic and oxidative reactions which have been implicated in various retinal pathologies and to highlight the contribution flavins may have played in these. Recent research has found a sensitive method of measuring flavins in both diseased and healthy retina, presence of a novel flavin binding protein exclusively expressed in the retina, and the presence of flavin specific transporters in both the inner and outer blood-retina barriers. In light of these exciting findings, it is even more imperative to shift our focus on how the retina regulates its flavin homeostasis and what happens when this is disrupted.

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Glucose in platelet additive solutions: To add or not to add?

Gyöngyössy‐Issa

2011

Transfusion and Apheresis Science

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Effects of riboflavin-2',3',4',5'-tetrabutyrate and flavin adenine dinucleotide on the platelet aggregation induced by hydrogen peroxide.

Cited by 7 publications

References 18 publications

Further studies on the effects of flavine adenine dinucleotide on the platelet functions.

Further studies on the effects of flavine adenine dinucleotide on the platelet functions.

Flavins Act as a Critical Liaison Between Metabolic Homeostasis and Oxidative Stress in the Retina

Glucose in platelet additive solutions: To add or not to add?

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