Calcium ion as a probe of the monovalent cation center of sodium, potassium ATPase.

Abstract Differences in volume, water content and weight of leukocytes of different morphologic type are described. These differences make it mandatory that the influence of those factors which contribute to the denominator in comparative studies of leukocyte characteristics be considered if different cell types are being compared. The influence of cell isolation on monovalent cation content is emphasized. Restoration of a high potassium, low sodium steady-state occurred at 37 C. after incubation in physiologic solutions. Inhibition of this cation restoration by ouabain, or deviations from optimal extracellular pH, optimal ambient temperature and optimal extracellular potassium concentration coupled with the presence of ouabain inhibitable monovalent cation activated adenosine triphosphate hydrolysis in vitro support the presence of active cation transport in all types of human leukocytes studied. It is likely that discrepant values for leukocyte cation content and absence of monovalent cation activated ATPase previously reported are related to technical factors. Leukemic and normal granulocytes and lymphocytes of similar morphologic type do not differ in their monovalent cation content or in sodium-potassium ATPase activity. Cell volume of leukemic and normal small lymphocytes and PMNG’s parallels their cation content. Immature granulocytes and small lymphocytes have higher sodium-potassium ATPase activities than mature granulocytes. Sodium concentration and water content were also slightly higher in immature granulocytes and lymphocytes as compared to PMNG’s. The data are consistent with the hypothesis that increased sodium-potassium ATPase activity is a biochemical feature of leukocytes with the potential to divide and differentiate. The impaired mitotic capacity of human leukemic blast cells does not appear to be related to a deficiency in sodium-potassium ATPase activity or a resultant alteration in intracellular monovalent cation content.

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Adenosine Receptor Modulation of Hypoxic-ischemic Injury in Striatum of Newborn Piglets

Current Neurovascular Research ◽

10.2174/1567202617999200831152233 ◽

2020 ◽

Vol 17 (4) ◽

pp. 510-517

Author(s):

Santiago Ortega-Gutierrez ◽

Brandy Jones ◽

Alan Mendez-Ruiz ◽

Pankhil Shah ◽

Michel T. Torbey

Keyword(s):

Oxidative Stress ◽

Atpase Activity ◽

Neuronal Injury ◽

Receptor Activation ◽

Adult Mortality ◽

Vehicle Group ◽

Sodium Potassium ◽

Receptor Modulation ◽

A2a Receptor ◽

Potassium Atpase

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na+, K+-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na+, K+-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na+, K+-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na+, K+-ATPase activity and increased oxidative stress.

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