Behavior of Serum Adenosine Deaminase and Its Isoenzymes in Patients with Urticaria (original) (raw)
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Rheumatology …, 2011
Adenosine deaminase (ADA) plays a crucial role in the development and maintenance of normal immune system. So, any immunological imbalances could associate with its altered activity in serum. This study evaluated the activity of total ADA and its isoenzymes in serum of 45 patients with systemic lupus erythematosus (SLE). Included were 23 patients with active SLE, 22 during the inactive phase of the disease, and 45 healthy subjects. Our results provided evidence that the signiWcantly elevated total ADA activity in serum of SLE patients is correlated mainly with the increased ADA2 level. The highest mean ADA2 activity during the relapse phase of the disease could be an indication to the macrophages, the main source of ADA2. It might be concluded that ADA and its isoenzymes analysis in serum of patients could be used as a useful and non-invasive diagnostic tool in evaluation of SLE active phase and the disease severity.
Iranian Journal of Parasitology, 2020
Background: Adenosine deaminase (ADA) is an aminohydrolase involved in the catabolism of purine nucleotides and irreversibly deaminizes adenosine and deoxyadenosine to inosine and deoxyinosine. ADA enzyme deficiency results in the loss of functional properties of B and T lymphocytes. Demodex species have been reported to be transmitted between humans through close contact and to play a role in the pathogenesis of rosacea, acne vulgaris, perioral dermatitis, seborrhoeic dermatitis, micropapillary-pruritic dermatitis and blepharitis. The present study aimed to compare serum ADA levels in D. folliculorum positive patients with the healthy control individuals. Methods: Serum ADA levels were examined for 30 patients diagnosed with erythematotelangiectatic rosacea and 40 healthy individuals in Malatya Inonu University in 2017. Standardized skin surface biopsy (SSSB) method was used to diagnose D. folliculorum. A significant decrease was found in the ADA levels of Demodex-positive rosacea ...
A Kinetic Comparison on the Inhibition of Adenosine Deaminase by Purine Drugs
Iranian Journal of Pharmaceutical Research, 2007
The effects of allopurinol, acyclovir and theophylline on the activity of adenosine deaminase (ADA) were studied in 50 mM sodium phosphate buffer pH 7.5 at 27 °C, using a UV– Vis spectrophotometer. Adenosine deaminase is inhibited by these ligands, via different types of inhibition. Allopurinol, as a transition state analog of xanthine oxidase, and acyclovir competitively inhibit the catalytic activity of ADA. Inhibition constant values are 285 and 231 µM for allopurinol and acyclovir, respectively. Theophylline acts as a non-competitive inhibitor for ADA, which shows different affinity binding sites at various drug concentrations. There were two different types of inhibition constant, one of them due to a low concentration of the drug (K i = 56 μM) and the other appearing at higher concentrations of theophylline (K i = 201 μM). Thermodynamic parameters also show that ADA has two binding sites for theophylline. The comparison of inhibition constant for inosine (K i = 143 μM) and acy...
Serum Adenosine Deaminase Activity in Domestic Animals: Reference Values
Turkish Journal of Veterinary & Animal Sciences
Adenosine deaminase (ADA, EC 3.5.4.4) is an enzyme that catalyses hydrolytic deamination of either adenosine or deoxyadenosine to produce inosine and deoxyinosine, respectively (1). Firstly, the presence of enzyme was detected in whole blood and serum by Conway and Cooke (2). In domestic animals, ADA is present in all organs, although the highest activity has been found in lymphoid tissues (3). In animals, ADA and its isoenzyme activities in the spleen, lymph nodes, and thymus have been found in high levels, and in the brain, adrenal gland, muscles, kidney, and liver in low level (4). It has been detected in 137
Novel Pathway of Adenosine Generation in the Lungs from NAD+: Relevance to Allergic Airway Disease
Molecules, 2020
Adenosine and uric acid (UA) play a pivotal role in lung diseases such as asthma and chronic obstructive pulmonary disease (COPD). In the present experiments, we measured adenosine synthesis from nicotinamide adenine dinucleotide (NAD+) in membranes prepared from wild type (WT) and CD38 knockout (CD38KO) mouse lungs, from cultured airway smooth muscle and epithelial cells, and in bronchoalveolar lavage fluid after airway challenge with epidemiologically relevant allergens. Adenosine was determined using an enzymatically coupled assay that produces ATP and is detected by luminescence. Uric acid was determined by ELISA. Exposure of cultured airway epithelial cells to Alternaria alternata extract caused significant nucleotide (NAD+ and ATP) release in the culture media. The addition of NAD+ to membranes prepared from WT mice resulted in faster generation of adenosine compared to membranes from CD38KO mice. Formation of adenosine from NAD+ affected UA and ATP concentrations, its main do...
Cytokines regulate membrane adenosine deaminase on human activated lymphocytes
2001
CD26 is a lymphocyte marker that can anchor adenosine deaminase (ADA) on the T cell surface. We found that ADA is regulated by cytokines on the cell surface during T cell activation. By means of flow cytometry, immunofluorescence, and immunoblotting techniques, we found that interleukin (IL)-2 and IL-12 up-regulate ecto-ADA and CD26 expression. In clear contrast, IL-4 led to down-regulation of lymphocyte surface ADA without modifying the level of CD26. Moreover, neither circulating ADA transcription nor mRNA translation was regulated by cytokines. These results, along with absence of total-ADA modulation, the variable amount of ADA found in purified plasma membranes, and the different effect of Brefeldin A on the surface presence of ADA and CD26 indicated that cytokines regulate the translocation of ADA towards the cell surface through a mechanism not involving CD26. Ecto-ADA protected activated lymphocytes from the toxic effects of extracellular adenosine. Therefore, this cell surface ADA control might constitute part of the fine immunoregulatory mechanism of adenosine-mediated signaling through purinergic receptors in leukocytes. J. Leukoc. Biol. 70: 920 -930; 2001.
Adenosine Deaminase Isoenzymes in the Diagnosis and Monitoring of Rheumatoid Arthritis
Journal of Medical Biochemistry, 2012
Adenosine Deaminase Isoenzymes in the Diagnosis and Monitoring of Rheumatoid ArthritisThe aim of this study was determination of the catalytic activities of adenosine deaminase (ADA), ADA1 and ADA2 isoenzymes in the serum of patients suffering from rheumatoid arthritis (RA) who were and were not treated with methotrexate (MTX), and identification of the possibilities of using these biochemical parameters in diagnosing and monitoring the treatment effects in RA. Catalytic activities of total ADA (tADA) and ADA2 in serum were determined by a spectrophotometric method. A statistically significant correlation was found between the total ADA and ADA1 values, as well as between tADA and ADA2 in the serum of all patients suffering from RA. Determination of ADA1 and ADA2 isoenzyme catalytic activities in the serum of patients who might be suffering from RA improves the diagnostic value of total ADA catalytic activity determination. ADA2 catalytic activity in serum can be a useful biochemica...
Evaluation of adenosine deaminase activity in patients with head and neck cancer
Journal of Surgical Research, 1986
ADA is a key enzyme in the mammalian purine salvage pathway. The lack of ADA activity has been linked to a lack of cellular immunity in various immune and myeloproliferative disorders. Data on its role in patients with solid tumors are scant and inconclusive. In this report, we have evaluated the activity of this enzyme in the peripheral lymphocytes of patients with head and neck squamous cell cancer (HNC). The mean ADA activity in Stage IV patients (0.57 + 0.08 SEM, II = 12) was significantly lower than that of controls (1.55 + 0.25 SEM, P < 0.05, n = 14) and also significantly lower that the mean ADA activity in patients with Stages I, II, and III (1.14 + 0.10 SEM, P < 0.05, n = 17). Fourteen out of 19 controls, Stage I, II, and III patients had positive skin tests compared to 7 out of 10 Stage IV patients. These differences were not statistically significant. There was also no correlation between ADA activity and the absolute lymphocyte counts. Our results indicate that ADA activity in lymphocytes of patients with advanced HNC is lower than that of controls or patients with earlier stages of the disease. ADA may be a more sensitive indicator of suppressed cellular immunity than delayed cutaneous hypersensitivity reactions, or monitoring absolute lymphocyte counts. Q