Post-thyroidectomy hypothyroidism increases the expression and activity of ectonucleotidases in platelets: Possible involvement of reactive oxygen species. (17th November 2018)

• Record Type: Journal Article
• Authors: Baldissarelli, Jucimara; Pillat, Micheli M.; Schmatz, Roberta; Cardoso, Andréia M.; Abdalla, Fátima H.; de Oliveira, Juliana S.; Polachini, Carla R. N.; Casali, Emerson; Bornemann, Clarissa Pereira; Ulrich, Henning; Morsch, Vera M.; Schetinger, Maria R. C.
• Is Part Of: Platelets. Volume 29:Number 8(2018)
• Page Start: 801
• Page End: 810
• Publication Date: 2018-11-17
• Subjects: Adenosine deaminase -- ectonucleotidases -- hypothyroidism -- oxidative stress -- platelets; Blood platelets -- Periodicals; Blood Platelets -- Periodicals; 615.39
• DOI: 10.1080/09537104.2017.1361017
• Languages: English
• ISSNs: 0953-7104

Abstract

Abstract: 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.