Ischemia-Reperfusion Injury in the Transplanted Kidney Based on Purine Metabolism Markers and Activity of the Antioxidant System

Plasma Hypoxanthine-Guanine Phosphoribosyl Transferase Activity in Bottlenose Dolphins Contributes to Avoiding Accumulation of Non-recyclable Purines

“…HGPRT activity in plasma of dolphins could offer an advantage to salvage and supply nucleotide precursors to cells or tissues that require returning to basal levels following an episode of ischemia and/or hypoxia. For example, it is possible that under ischemic/hypoxic conditions, nucleosides and oxypurines are released to plasma, a fraction of purines are delivered directly to RBC to produce new nucleosides and nucleotides (Dománski et al, 2012 ). High permeability of RBC from bottlenose dolphins and humans to nucleosides and glucose (Craik et al, 1997 ) could ensure suitable levels of adenine and guanine nucleotides inside these cells.…”

Purinergic signaling and purine base metabolism at the crossroads between immunity, metabolism, and cancer: A review

“…Other groups who interrogated the role of purines in GVHD found that transplant regimens commonly induced the release of danger‐associated molecular patterns (DAMPs) such as ATP, and that ATP can bind to purinergic receptors on T‐cells to promote a pro‐inflammatory microenvironment that exacerbates GVHD; however, the concentration of ATP and the activation of different purinergic receptors will dictate outcomes 109 . The purine metabolism enzyme xanthine oxidase (XO) generates ROS that cause the cellular damage and inflammation associated with ischemia‐reperfusion injury, 112–114 while CD39, CD73, P1 receptors, and P2 receptors have all been implicated in the development of GI inflammation and IBD 117 . Progression of the autoimmune demyelinating disease, MS, is associated with differential expression of three purinergic receptors on microglial cells; P2Y12 is increased in control cells and decreases over the course of disease as chemotaxis is reduced, while P2 × 7 and P2 × 4 are both increased at the site of MS lesions and promote detrimental inflammasome activation and beneficial myelin phagocytosis, respectively 123 .…”

“…Defects in purine signaling and metabolism have been wellcharacterized in several inflammatory diseases including lung disorders such as asthma [98][99][100][101][102] or chronic obstructive pulmonary disease (COPD), [103][104][105][106][107] graft-versus-host-disease (GVHD), [108][109][110][111] ischemiareperfusion injury, [112][113][114][115][116] gastrointestinal (GI) inflammation or inflammatory bowel disorder (IBD) [117][118][119][120][121][122] multiple sclerosis (MS), [123][124][125][126][127] and myasthenia gravis, 128,129 among others. Inflammatory disorders in the airway are mediated in part by both enhanced levels of adenosine in the bronchoalveolar lavage fluid and by enhanced hyperresponsiveness to adenosine challenge.…”

“…generates ROS that cause the cellular damage and inflammation associated with ischemia-reperfusion injury, [112][113][114] while CD39, CD73, P1 receptors, and P2 receptors have all been implicated in the development of GI inflammation and IBD. 117 Progression of the autoimmune demyelinating disease, MS, is associated with differential expression of three purinergic receptors on microglial cells; P2Y12 is increased in control cells and decreases over the course of disease as chemotaxis is reduced, while P2 × 7 and P2 × 4 are both increased at the site of MS lesions and promote detrimental inflammasome activation and beneficial myelin phagocytosis, respectively.…”