Effect of anethole dithiolthione on human platelet aggregation

Arzneimittelforschung. 1992 Mar;42(3):318-21.

Abstract

Anethole dithiolthione (ADT) (10 mumol/l) inhibited platelet aggregation and the formation of thromboxane (Tx)B2 in plasma in response to adenosine diphosphate (ADP), epinephrine and arachidonic acid (AA). ADT partially inhibited platelet aggregation and TxB2 formation in plasma induced by thrombin, phorbol myristate acetate and calcium ionophore A23187 and increased the lag time of collagen-induced aggregation at concentrations in the range 10-40 mumol/l. ADT (100 mumol/l) completely inhibited the aggregation of washed platelets challenged with thrombin. ADT had no additive effect on the inhibition of thrombin-induced platelet aggregation by acetylsalicylic acid. ADT was a more effective inhibitor of AA-induced platelet aggregation than butylated hydroxytoluene. ADT inhibited the release of 3H-AA from platelet phospholipids in response to ADP and collagen. It is suggested that ADT inhibits platelet aggregation by inhibiting thromboxane synthesis and preventing AA release.

MeSH terms

  • Adenosine Diphosphate / pharmacology
  • Adult
  • Anethole Trithione / pharmacology*
  • Arachidonic Acid / blood
  • Aspirin / pharmacology
  • Butylated Hydroxytoluene / pharmacology
  • Humans
  • In Vitro Techniques
  • Platelet Aggregation / drug effects*
  • Platelet Aggregation Inhibitors / pharmacology*
  • Radioimmunoassay
  • Thrombin / pharmacology
  • Thromboxane B2 / blood

Substances

  • Platelet Aggregation Inhibitors
  • Butylated Hydroxytoluene
  • Arachidonic Acid
  • Thromboxane B2
  • Adenosine Diphosphate
  • Thrombin
  • Anethole Trithione
  • Aspirin