Scavenger là gì

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Affiliation

1 Medicina Interna ed Oncologia Medica, Università degli Studi di Pavia, IRCCS Policlinico San Matteo, 27100 Pavia, Italy. c.porta


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Amifostine, a reactive oxigen species scavenger with radiation- và chemo-protective sầu properties, inhibits in vitro platelet activation induced by ADPhường, collagen or PAF

Affiliation

1 Medicina Interna ed Oncologia Medica, Università degli Studi di Pavia, IRCCS Policliniteo San Matteo, 27100 Pavia, Italy. c.porta

Background & objectives: Reactive oxygene species (ROS) generation has been suggested khổng lồ represent an important regulatory mechanism of platelet reactivity in both physioxúc tích và ngắn gọn and pathoxúc tích và ngắn gọn conditions; consistent with this hypothesis is the observation that free-radical scavengers may inhibit platelet activation, thus contributing to the regulation of their reactivity. The purpose of the present study is to study the in vitro effects of amifostine (WR-2721, ethyol ), a selective sầu cytoprotective sầu agent for normal tissues against the toxicities of chemotherapy & radiation, on platelet activation induced by the physioxúc tích agonists ADPhường., collaren and PAF.

Design và methods: The effect of amifostine, added lớn the experimental system at final concentrations ranging from 10(-7) M lớn 10(-5) M, was studied on platelet aggregation induced by the following physiosúc tích agonists at the given concentrations: ADPhường (1 microM), collagene (2 microg/mL), và PAF (0.1 microg/mL). Platelet aggregation was investigated using a platelet ionized calcium aggregometer and was expressed as the percentage change in light transmission. Furthermore, thromboxane B((2)) (TxB((2))) levels and nitric oxide (NO) production were determined by radioimmunoassay and by evaluating the total nitrite/nitrate concentration using a commercially available colorimetric kit, respectively, both in the control system & after the addition of amifostine.

Results: Amifostine inhibited both platelet aggregation và TxB((2)) production induced by ADPhường, collaren and PAF, in a dose-dependent manner.

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Amifostine proved to lớn be an effective inhibitor of platelet function & the effect was more pronounced if platelets were stimulated with ADPhường, intermediate when collagene was the chosen agonist, and less evident, though present, when PAF was used. Platelets stimulated with ADPhường, collaren or PAF produced significant amounts of NO over the baseline. When amifostine was added at a final concentration of 5 microM, it significantly increased ADP, collagene and PAF-induced NO production, which suggests that NO release by activated platelets was involved in the inhibitory effect of amifostine.

Interpretation and conclusions: Amifostine proved khổng lồ be an effective sầu inhibitor of platelet activation induced in vitro by physiolô ghích inducers. This previously unrecognized effect was more evident with the weak agonist ADPhường. and was related lớn reduced NO consumption by free radicals generated during platelet activation. Amifostine proved to be not only a powerful cytoprotectant, but, more generally, a therapeutic agent endowed with several relevant, though largely unknown, biological effects. Finally, our data once again tư vấn the concept that oxidative balance is of crucial importance in regulating platelet reactivity in both health and disease.


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