[Lipopolysaccharide composition of wild P678 and mutant PM61 strains of Escherichia coli K12].
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Biomedical subjects
Publications and source records attributed to D Blache.
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We investigated whether changes in plasma oxidative properties could occur after oral (hormonal) contraceptive (OC) administration in female rats and whether such changes could be responsible for the platelet increase in aggregation and lipid biosynthesis observed with that treatment. Platelets and plasma (platelet-poor) from control and OC (ethinyl estradiol + lynestrenol)-treated rats were prepared separately. Thrombin-induced aggregation of control platelets was markedly enhanced after incubation for 4 (p less than 0.025) to 60 (p less than 0.001) minutes in OC as compared with control plasma. Under the same conditions, platelet lipid biosynthesis was increased also (p less than 0.05 to p less than 0.01), but after 3 hours incubation. The enhanced response of platelets to aggregation induced by OC plasma could be inhibited by adding either glutathione (p less than 0.025), vitamin E (p less than 0.025), catalase (p less than 0.05), or peroxidase + glutathione (p less than 0.005) to plasma or 2,6,di-bis(ter-butyl)p-cresol (p less than 0.05) to platelets before incubation. The peroxidized free fatty acids isolated from OC plasma added to normal platelets induced a 150% (p less than 0.001) increase in the response to thrombin as compared with the fatty acids from control plasma. In addition, the level of malondialdehyde and conjugated dienes was significantly (p less than 0.02 to p less than 0.001) increased in OC compared with control plasma. We conclude that the enhanced formation in plasma of lipid hydroperoxides seems to be the initial event stimulating platelets after OC treatment, at least in rats.
Blood platelets are discoid cellular fragments without nucleus originating from megakaryocytes. Platelets are able to respond to a great variety of agonists which bind to specific receptors localized on the plasma membrane. This process takes place when blood vessels are cut. Platelets then change their shape, adhere to newly exposed subendothelial tissues, release the content of numerous secretory granules and aggregate together. During this process, a great numbers of biochemical reactions are triggered such as phospholipases activation, synthesis of mediators and protein phosphorylation. These events result from increased cytoplasmic free calcium originating through calcium channels from the extracellular medium and from internal stores. Involvement of blood platelets in cardiovascular diseases may result from an exaggeration of these mechanisms by risk factors and are also discussed.