Why the study?
Does a complex between bacterial endotoxin and copper (Cu2+) induce platelet aggregation in mammalian blood platelets?
Does a complex between bacterial endotoxin and copper (Cu2+) induce platelet aggregation in mammalian blood platelets?
A specific complex between bacterial endotoxin and copper induces a unique pathway of platelet aggregation independent of ADP or collagen.
Endotoxin-Cu2+ may trigger a distinct platelet pathway in mammals; leaves open any role in human sepsis or thrombosis.
The presence of a complex formed between bacterial endotoxin and cupric ion (Cu2+) causes mammalian (human, pig, and rabbit) blood platelets to aggregate in suspension. Complexes formed between endotoxin and Zn2+, Co2+, Ni2+, Mn2+, Fe3+, Ca2+, Mg2+, Ba2+, Al3+, Be2+, Pb2+, Cd2+, Ag+, or Hg2+ do not cause aggregation. The initial stage of the aggregation induced by the complex is not inhibited by inhibitors of adenosine diphosphate (ADP) or collagen induced aggregation, and is not accompanied by release of measureable amounts of serotonin or ADP. The potential clinical significance of the phenomenon is noted.
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Lewis et al. (1971) studied this question.
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