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首页> 外文期刊>Platelets >Cigarette smoke inhibits adenine nucleotide hydrolysis by human platelets.
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Cigarette smoke inhibits adenine nucleotide hydrolysis by human platelets.

机译：香烟烟雾抑制人血小板的腺嘌呤核苷酸水解。

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Cigarette smoking is a recognized risk factor for cardiovascular diseases and has been implicated in the pathogenesis of atherosclerosis and thrombotic events. In athero-thrombotic diseases, the extracellular adenine nucleotides play an important role by triggering a range of effects such as the recruitment and activation of platelets, endothelial cell activation and vasoconstriction. NTPDase, a plasma membrane-bound enzyme, is the most relevant enzyme involved in the hydrolysis of extracellular tri- and di-phosphate nucleotides to adenosine monophosphate, which is further degraded by 5'ectonucleotidase to the anti-thrombotic and anti-inflammatory mediator adenosine. Thus, the preserved activity of these enzymes, regulating the extracellular concentrations of nucleotides, is critical in thromboregulatory functions. In the present in vitro study, performed on human platelets suspended in undiluted or diluted aqueous cigarette smoke extract (aCSE), we demonstrated that undiluted and 1 : 2 diluted aCSE isable to significantly reduce ADP hydrolysis (-24% and 12%, respectively) by intact human platelets. ATP degradation was also reduced (-31%) by undiluted aCSE. Conversely, aCSE did not alter platelet AMP hydrolysis. Results obtained by using N-acetylcysteine, a thiol-containing antioxidant, suggest that stable oxidants present in aCSE are responsible for the platelet NTPDase inhibition induced by aCSE. The decreased adenine nucleotide degradation could play a significant role in the extensive platelet activation and vascular inflammation observed in chronic smokers.
机译：吸烟是公认的心血管疾病危险因素，与动脉粥样硬化和血栓形成的发病机理有关。在动脉血栓形成疾病中，细胞外腺嘌呤核苷酸通过触发一系列作用（例如募集和激活血小板，内皮细胞激活和血管收缩）起重要作用。 NTPDase是一种与质膜结合的酶，是与胞外三磷酸和二磷酸核苷酸水解为单磷酸腺苷有关的最相关酶，单磷酸经5'外切核苷酸酶进一步降解为抗血栓和抗炎介质。因此，调节这些酶的细胞外浓度的这些酶的保留活性在血栓调节功能中至关重要。在目前的体外研究中，对悬浮在未稀释或稀释的卷烟烟雾提取物（aCSE）中的人类血小板进行的研究表明，未稀释和1：2稀释的aCSE能够显着降低ADP水解（分别为-24％和12％）通过完整的人类血小板。未稀释的aCSE也可降低ATP降解（-31％）。相反，aCSE不会改变血小板AMP的水解。通过使用N-乙酰半胱氨酸（一种含硫醇的抗氧化剂）获得的结果表明，aCSE中存在的稳定氧化剂是aCSE诱导的血小板NTPDase抑制的原因。减少的腺嘌呤核苷酸降解可能在慢性吸烟者中观察到的广泛的血小板活化和血管炎症中起重要作用。

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