Redox Biology | |
Purinergic signaling in the modulation of redox biology | |
Raíssa Leite-Aguiar1  Robson Coutinho-Silva2  Vinícius Santos Alves2  Luiz Eduardo Baggio Savio2  Angela T.S. Wyse2  | |
[1] Corresponding author. Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Edifício do Centro de Ciências da Saúde, Bloco G. Av. Carlos Chagas Filho, 373. Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ, 21941-902, Brazil.;Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil; | |
关键词: Oxidative stress; ROS; ATP; P2 receptors; Ectonucleotidases; Adenosine; | |
DOI : | |
来源: DOAJ |
【 摘 要 】
Purinergic signaling is a cell communication pathway mediated by extracellular nucleotides and nucleosides. Tri- and diphosphonucleotides are released in physiological and pathological circumstances activating purinergic type 2 receptors (P2 receptors): P2X ion channels and P2Y G protein-coupled receptors. The activation of these receptors triggers the production of reactive oxygen and nitrogen species and alters antioxidant defenses, modulating the redox biology of cells. The activation of P2 receptors is controlled by ecto-enzymes named ectonucleotidases, E-NTPDase1/CD39 and ecto-5’-nucleotidase/CD73) being the most relevant. The first enzyme hydrolyzes adenosine triphosphate (ATP) and adenosine diphosphate (ADP) into adenosine monophosphate (AMP), and the second catalyzes the hydrolysis of AMP to adenosine. The activity of these enzymes is diminished by oxidative stress. Adenosine actives P1 G-coupled receptors that, in general, promote the maintenance of redox hemostasis by decreasing reactive oxygen species (ROS) production and increase antioxidant enzymes. Intracellular purine metabolism can also contribute to ROS generation via xanthine oxidase activity, which converts hypoxanthine into xanthine, and finally, uric acid. In this review, we describe the mechanisms of redox biology modulated by purinergic signaling and how this signaling may be affected by disturbances in the redox homeostasis of cells.
【 授权许可】
Unknown