腺苷
活性氧
腺苷脱氨酶
内分泌学
化学
内科学
TBARS公司
三磷酸腺苷
嘌呤能信号
血小板
氧化应激
谷胱甘肽
嘌呤
生物化学
生物
医学
脂质过氧化
酶
腺苷受体
受体
兴奋剂
作者
Jucimara Baldissarelli,Micheli Mainardi Pillat,Roberta Schmatz,Andréia Machado Cardoso,Fátima Husein Abdalla,Juliana Sorraila de Oliveira,Carla Roberta Nunes Polachini,Émerson André Casali,Clarissa Pereira Bornemann,Henning Ulrich,Vera Maria Morsch,Maria Rosa Chitolina Schetinger
出处
期刊:Platelets
[Informa]
日期:2017-11-01
卷期号:29 (8): 801-810
被引量:8
标识
DOI:10.1080/09537104.2017.1361017
摘要
Signaling mediated by purines is a widespread mechanism of cell-cell communication related to vasomotor responses and the control of platelet function in the vascular system. However, little is known about the involvement of this signaling as well as the role of reactive oxygen species (ROS) in the development of hypothyroidism. Therefore, the present study investigates changes in the purinergic system, including enzyme activities and expression in platelets, and oxidative profiles in patients with post-thyroidectomy hypothyroidism. The nucleoside triphosphate diphosphohydrolase 1 (NTPDase/CD39) expression in patients increased by 40%, and the adenosine triphosphate (ATP) or adenosine diphosphate (ADP) hydrolyzing activity increased by 82% and 70%, respectively. The activities of ecto-5´-nucleotidase and adenosine deaminase (ADA) also significantly enhanced (39% and 52%, respectively), which correlates with a 45% decrease in adenosine concentration. Furthermore, these patients demonstrated an increased production of ROS (42%), thiobarbituric acid reactive substances (TBARS) (115%), carbonyl protein (30%) and a decreased glutathione S-transferase (GST) activity (20%). This study demonstrates that hypothyroidism interferes with adenine nucleoside and nucleotide hydrolysis and this is correlated with oxidative stress, which might be responsible for the increase in ADA activity. This increase causes rapid adenosine deamination, which can generate a decrease in their concentration in the systemic circulation, which can be associated with the development of vascular complications.
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