Kinetic study of adenosine concentrations and the expression of adenosine deaminase in mononuclear cells during hemodialysis

Dussol, Bertrand; Fenouillet, Emmanuel; Brunet, Phillippe; Purgus, Radj; Sauze, Nicole; Carrega, Louis; Mercier, Laurence; Ibrahim, Zein Shaban; Bechis, Guy; Berland, Yvon; Guieu, Régis

doi:10.1111/j.1523-1755.2004.00930.x

Cited by 18 publications

(15 citation statements)

References 33 publications

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“…The observed decrease of total (cytoplasmic and cell surface CD26 associated) ADA activity is in agreement with the enhancement of adenosine metabolism and fits very well with previous studies which revealed inhibition of ADA and adenosine kinase as a metabolic adaptation to elevated adenosine levels in rat pheochromocytoma (PC12) cells chronically exposed to hypoxia [7]. High adenosine levels with decreased ADA activity were also observed in mononuclear cells of hemodialysed patients with immune defect [11]. In contrast, hypoxia was reported to increase total and cell surface ADA protein level and enzymatic activity in cultured endothelial cells [24].…”

Section: Hypoxia-adenosinergic Mechanismsupporting

confidence: 78%

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Fall in oxygen tension of culture medium stimulates the adenosinergic signalling of a human T cell line

Jacquin

Franceschi

et al. 2012

Purinergic Signalling

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We examined the short-course expression of various parameters involved in the adenosinergic signalling of a human T cell line during in vitro decrease of the medium culture oxygen tension mimicking in vivo hypoxia. Fall of 92 mmHg in oxygen tension of culture medium induced in CEM, a CD4+ human T cell line, a continuous production of hypoxia-inducing factor-1α with a plateau value at 9 h, a rapid increase in adenosine production peaking at 3 h and a decrease in adenosine deaminase peaking at 6 h. The adenosine A 2A receptor (A 2A R) protein level of CEM cells was enhanced with a peak at 6 h. Intracellular 3′,5′-cyclic adenosine monophosphate accumulated in CEM cells with a maximal level at 9 h. These results show that a humancultured T cells line can upregulate its own adenosine production and A 2A R expression during exposure to acute hypoxia. Hypoxia-increased stimulation of the adenosinergic signalling of T cells may have immunosuppressive properties and, consequently, A 2A R agonists may have therapeutic relevance.

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Section: Hypoxia-adenosinergic Mechanismsupporting

confidence: 78%

“…Adenosine deaminase (ADA) activity measurement was carried out as previously described [11]. Briefly, 1×10 6 frozen cells were lysed in 500 μl of ultrapure water.…”

Section: Ada Activitymentioning

confidence: 99%

Fall in oxygen tension of culture medium stimulates the adenosinergic signalling of a human T cell line

Jacquin

Franceschi

et al. 2012

Purinergic Signalling

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“…APLs can also be increased in patients with chronic renal failure, but this increase has been observed only in patients with end-stage renal failure under haemodialysis treatment 35 36…”

Section: Discussionmentioning

confidence: 99%

Peripheral plasma adenosine release in patients with chronic heart failure

Franceschi

Deharo

Giorgi

et al. 2008

Heart

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“…After incubation (37°C, for 30 min), uric acid was evaluated using a DX Beckman Coulter apparatus [35]. ADO and ADA plasma concentrations were measured as described previously [36]. Briefly for ADO, a Hewlett Packard HP 1100 modular system with a diode array detector was used (Hewlett Packard, Palo Alto, Calif., USA).…”

Section: Methodsmentioning

confidence: 99%

Plasma Xanthine Oxidase Activity Is Predictive of Cardiovascular Disease in Patients with Chronic Kidney Disease, Independently of Uric Acid Levels

Gondouin

Jourde-Chiche

Sallée

et al. 2015

Nephron

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Background: Chronic kidney disease (CKD) is associated with increased cardiovascular morbidity and mortality. Oxidative stress seems to play a pivotal role in this process, and purine metabolism may be involved in CKD-related oxidative stress. Xanthine oxidase (XO) is an enzyme involved in purine metabolism and is also responsible for the production of reactive oxygen species. Methods: This prospective study aimed to analyze the relation between plasma dosages of molecules involved in redox balance, purine metabolism and cardiovascular events in patients with non-diabetic CKD stages 3-5 or on chronic hemodialysis (HD). CKD (n = 51) and HD (n = 50) patients were compared to matched healthy controls (n = 38) and followed-up for 3 years. Results: Both CKD and HD patients had decreased plasma levels of antioxidants (selenium, zinc, vitamin C). HD patients had decreased levels of the antioxidant enzyme superoxide dismutase and increased levels of oxidation products (ischemia-modified albumin, malondialdehyde [MDA]). The following substrates and enzymes involved in purine metabolism were increased in the HD cohort: adenosine, adenosine deaminase and the pro-oxidant XO. XO activity was negatively correlated with super oxide dismutase and positively with MDA. Interestingly, XO activity was an independent predictor of cardiovascular events in CKD and HD patients, regardless of uric acid levels. Uric acid was not predictive of events. Conclusion: This highlights a possible role of XO itself in CKD-related cardiovascular disease (CVD) and raises the hypothesis that beneficial effects observed with XO inhibitors on CVD in CKD may also be due to the reduction of oxidative stress.

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Kinetic study of adenosine concentrations and the expression of adenosine deaminase in mononuclear cells during hemodialysis

Abstract: HD affects the transcription of the gene encoding MCADA after just three HD sessions, leading to decreased MCADA activity and increased plasma concentration of Ado.

Cited by 18 publications

References 33 publications

Fall in oxygen tension of culture medium stimulates the adenosinergic signalling of a human T cell line

Fall in oxygen tension of culture medium stimulates the adenosinergic signalling of a human T cell line

Peripheral plasma adenosine release in patients with chronic heart failure

Plasma Xanthine Oxidase Activity Is Predictive of Cardiovascular Disease in Patients with Chronic Kidney Disease, Independently of Uric Acid Levels

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