Sequential effects of the thiol-oxidizing agent, diamide, on human platelets

Patscheke, Heinrich; Wörner, P.

doi:10.1016/0049-3848(78)90250-5

Cited by 16 publications

(7 citation statements)

References 19 publications

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“…These changes in the sulfhydryl-disulfide status of the cell have been shown to alter the transport of amino acids (29,30) and sugars (30,31). In human platelets, diamide treatment produced a stimulation of the hexose monophosphate shunt (32), increased glucose transport (33), altered platelet aggregation (34)(35)(36), and produced changes in cytoskeletal proteins (37). In the present study the effects of diamide on platelet function have been extended to the 5-HT transport system, where this sulfhydryl oxidizing agent was found to stimulate 5-HT uptake in a concentration-dependent manner (Table 1).…”

Section: Discussionmentioning

confidence: 80%

Stimulation of the active transport of serotonin into mouse platelets by the sulfhydryl oxidizing agent diamide

Bosin

Kasper

1992

J. Biochem. Toxicol.

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The purpose of this study was to determine the effects of diamide, a reversible sulfhydryl oxidizing agent, on the transport of serotonin (5-HT) by mouse platelets. Diamide produced a concentration-dependent (10-200 microM) stimulation of 5-HT transport that was rapid and sustained over 0-10 minutes of incubation. When platelets were incubated with diamide (10-200 microM) in the presence of glucose, the content of reduced glutathione was significantly decreased only at a final concentration of 200 microM, while washed platelets incubated with diamide (10-200 microM), in the absence of glucose, had a significant concentration-dependent decrease in their content of reduced glutathione. Fluoxetine, an inhibitor of the platelet 5-HT transporter, blocked diamide-induced stimulation of 5-HT transport. The kinetics of 5-HT transport showed that diamide caused a marked increase in the maximal rate of transport (Vmax control = 28.4 +/- 1.4 vs. Vmax diamide = 60.9 +/- 4.1 pM/10(8) platelets/4 min) but did not significantly alter the Km values. Ouabain, an inhibitor of platelet Na(+)-K+ ATPase, blocked the stimulation by diamide in a concentration-dependent manner. Dithiothreitol, a disulfide reducing agent, was able to partially reverse the stimulation of platelet 5-HT transport caused by diamide. This study has shown that diamide can stimulate the active transport of 5-HT by mouse platelets and suggests a possible role for free sulfhydryl groups in the regulation of this process.

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Section: Discussionmentioning

confidence: 80%

Stimulation of the active transport of serotonin into mouse platelets by the sulfhydryl oxidizing agent diamide

Bosin

Kasper

1992

J. Biochem. Toxicol.

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“…Recently, it has been shown that extracts of feverfew inhibit blood platelet aggregation and exocytotic activity in platelets and PMNL (3) and this may be relevant to the possible benefit of feverfew in clinical situations. It is known that agents that oxidizes cellular sulphydryl groups impair the behaviour of platelets (4,5) and PMNL (6)(7)(8) and we have already provided evidence that the effects of feverfew on platelet behaviour are via such a mode of action (9). In the present study, we have investigated the effect of an extract of feverfew on the phagocytic activity of PMNL and on PMNL aggregation and chemiluminescence generation.…”

Section: Introductionmentioning

confidence: 91%

Inhibition of the Behaviour of Human Polynuclear Leukocytes by an Extract ofChrysanthemum parthenium

Lösche¹,

Michel²,

Heptinstall³

et al. 1988

Planta Med

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Extracts of the leaves of Chrysanthemum parthenium (feverfew) inhibit the secretory activity of human blood platelets and polymorphonuclear leukocytes (PMNL) and it has been suggested that the inhibitory effect on platelets is mediated by a neutralization of cellular sulphydryl groups. The results indicate that the effect of feverfew) on PMNL behaviour may be via blockade of sulphydryl groups in the cells.Venous blood from healthy volunteers was collected into 1/10 volume of 0.1 M trisodium citrate dihydrate as anti-coagulant. The blood was centrifuged for 15 minutes at 250 g and the supernatant plasma was discarded. To each 1 ml of the cell sediment, 2 ml of PBS [that contained 5.5 mM glucose, 0.5% (w/v) bovine serum albumin (BSA), and 0.01 mM trisodium citrate dihydrate], 1 ml of 6% (wtv) dextrane solution (Infukoll 70, Arzneimittelwerk Dresden, GDR) and 3 U heparin were Downloaded by: Universite Laval. Copyrighted material.

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“…Diamide causes remarkable changes in blood platelet aggregation and release reac tion which is supposed to be a result of its action on platelet GSH level [8,13,14]. During the treatment of PRP with 500 «M diamide, a continuous oxidation of platelet GSH occurred, whereas the protein SH group content was decreased to 10-15%>.…”

Section: Discussionmentioning

confidence: 99%

“…In two experiments the effect of 500pM diamide on GSH and protein SH group con 14.5 m/W Tris-HCI buffer pH 7.4, the platelet pel let was suspended in 1.5 mM TNBS in 14.5 mA/ Tris-HCI buffer pH 7.4 and incubated under gen tle agitation for 60 min at 37 °C. Thereafter the platelets were sedimented by centrifugation, the lipids extracted and analyzed for labeled PE ac cording to Schick et al [17].…”

Section: Effect Of Diamide On Platelet Sh Groupsmentioning

confidence: 99%

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The Effect of Diamide (Azodicarboxylic Acid-<i>bis</i>-Dimethylamide) on Sulfhydryl Group Content, Proteins, and the Location of Phosphatidylethanolamine in Human Blood Platelets

Ostermann¹,

Spangenberg²,

Meyer

et al. 1982

Acta Haematol

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Treatment of human blood platelets with the thiol-oxidizing agent, diamide, causes rapid oxidation of glutathione and alterations in aggregation and release reaction. Moreover, cross-linking of proteins was observed. Three high molecular weight bands of 200 – 240 × 10³ daltons and a band of 66 × 10³ daltons were involved in this process. After reduction with dithiotreitol the normal pattern was received. In contrast to the erythrocyte, the cross-linking of platelet proteins was not accompanied by a reorientation of phosphatidylethanolamine in the membrane. Also a considerably smaller effect of diamide on platelet protein sulfhydryl group content was measured.

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Sequential effects of the thiol-oxidizing agent, diamide, on human platelets

Cited by 16 publications

References 19 publications

Stimulation of the active transport of serotonin into mouse platelets by the sulfhydryl oxidizing agent diamide

Stimulation of the active transport of serotonin into mouse platelets by the sulfhydryl oxidizing agent diamide

Inhibition of the Behaviour of Human Polynuclear Leukocytes by an Extract ofChrysanthemum parthenium

The Effect of Diamide (Azodicarboxylic Acid-<i>bis</i>-Dimethylamide) on Sulfhydryl Group Content, Proteins, and the Location of Phosphatidylethanolamine in Human Blood Platelets

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