Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The measurement of the nucleoside deaminases--cytidine deaminase, guanosine deaminase and adenosine deaminase--by reversed phase high performance liquid chromatography is reviewed. The clinical value of assaying the enzyme activity is discussed for each of these enzymes. Both cytidine deaminase and adenosine deaminase measurements have proven clinical value, although the use of the assay of cytidine deaminase in the diagnosis of pre-eclampsia is probably not helpful.
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PMID:The measurement of nucleoside deaminases by high performance liquid chromatography and their use in clinical chemistry. 176 May 90

The present study investigated serum adenosine deaminase (ADA) activity and the patterns of two ADA isoenzymes, ADA1 and ADA2, and to evaluate the possible role of cell-mediated immunity as causes of the changes in ADA activity in pre-eclampsia. We measured serum activities of total ADA, ADA1 and ADA2 in pre-eclampsia (n = 22) and normal pregnancy (n = 22). Peripheral blood monocyte counts and neopterin levels, reflecting the activation of the monocyte-macrophage cell system, were also measured. In pre-eclampsia, serum total ADA and ADA2 activities were significantly increased compared with normal pregnancy (p < 0.05), which were accompanied by increases in serum neopterin levels. These results suggest that increased total ADA activity reflects increases in ADA2 activity, which may be in part related to enhanced cell-mediated immunity during pre-eclampsia.
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PMID:Serum adenosine deaminase activity in women with pre-eclampsia. 1257 39

The aim of this study was to evaluate maternal-fetal plasma adenosine deaminase, xanthine oxidase (ADA, XO) activity and malondialdehyde (MDA) levels and the relationship between them in pre-eclampsia. Maternal and umbilical cord whole blood samples were taken from 29 pre-eclamptic and 33 normal pregnants. The plasma ADA, XO activities as well as MDA levels were assayed by spectrophotometric methods. MDA levels and ADA, XO activities were found to be higher in maternal and fetal plasma in pre-eclamptics than in normal pregnancy. The differences were statistically significant between groups (p < 0.05). Increased maternal-fetal plasma XO and ADA activities, as a marker of immunological disorder, may be related to the pathogenesis of pre-eclampsia. In addition, increased MDA levels may be a reflection of increased oxidative stress in pre-eclamptics and their fetuses.
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PMID:Maternal and fetal plasma adenosine deaminase, xanthine oxidase and malondialdehyde levels in pre-eclampsia. 1551 22

This study evaluated the relationship between the activity of the inflammatory indicator adenosine deaminase (ADA) in placental tissue and maternal and fetal (umbilical cord) plasma and the severity of pre-eclampsia. Maternal and umbilical vein whole blood and placental tissue samples were collected from women with normal pregnancies (n = 33) and patients with mild (n = 12) or severe (n = 17) preeclampsia. ADA activity was measured spectrophotometrically. Significantly increased ADA activity was detected in maternal and fetal plasma, and placental tissue in patients with mild and severe pre-eclampsia compared with normal pregnancies; there were no significant differences between the mild and severe cases. The presence of increased ADA activity in pre-eclampsia is consistent with activation of the inflammatory system in this condition. The increased ADA activity was related to the presence of the disease but not the severity of clinical symptoms. Neonatal outcome did not significantly correlate with observed ADA activity.
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PMID:Clinical correlation between adenosine deaminase activity and pre-eclampsia severity. 1686 18

We aimed to evaluate whole blood adenosine deaminase (ADA), myeloperoxidase (MPO), butyrylcholinesterase (BChE), and acetylcholinesterase (AChE) activities and to investigate whether there was a correlation between these enzymes and severity of preeclampsia and neonatal outcomes. Sixty-one pregnant women with mild (n = 31) or severe (n = 30) preeclampsia and 50 healthy controls were included in this study. Whole blood adenosine deaminase, myeloperoxidase, butyrylcholinesterase, and acetylcholinesterase activities were measured. Adenosine deaminase and myeloperoxidase activities were significantly higher in both mild and severe preeclamptic women than they were in the controls. There was also a significant difference between the severe and the mild preeclamptic groups with respect to these enzyme activities. Although BChE activity was lower in the severe preeclamptic women than it was in the healthy controls (P < .05), AChE activity was similar in all groups (P > .05). We noted an inverse correlation between ADA activity and birth weight (r = -0.337) (P < .05) and between MPO activity and Apgar scores at 1 and 5 minutes (r = -0.438 and r = -0.475, respectively, P < .01). We concluded that elevated ADA and MPO but not AChE activities may correlate with disease severity and neonatal outcomes in preeclamptic women. Further studies are needed to elucidate the exact roles of ADA and MPO in the pathophysiology of preeclampsia.
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PMID:Evaluation of the relationship between adenosine deaminase, myeloperoxidase, cholinesterase, preeclampsia severity, and neonatal outcomes. 2268 31

Preeclampsia is a prevalent pregnancy hypertensive disease with both maternal and fetal morbidity and mortality. Emerging evidence indicates that global placental DNA hypomethylation is observed in patients with preeclampsia and is linked to altered gene expression and disease development. However, the molecular basis underlying placental epigenetic changes in preeclampsia remains unclear. Using 2 independent experimental models of preeclampsia, adenosine deaminase-deficient mice and a pathogenic autoantibody-induced mouse model of preeclampsia, we demonstrate that elevated placental adenosine not only induces hallmark features of preeclampsia but also causes placental DNA hypomethylation. The use of genetic approaches to express an adenosine deaminase minigene specifically in placentas, or adenosine deaminase enzyme replacement therapy, restored placental adenosine to normal levels, attenuated preeclampsia features, and abolished placental DNA hypomethylation in adenosine deaminase-deficient mice. Genetic deletion of CD73 (an ectonucleotidase that converts AMP to adenosine) prevented the elevation of placental adenosine in the autoantibody-induced preeclampsia mouse model and ameliorated preeclampsia features and placental DNA hypomethylation. Immunohistochemical studies revealed that elevated placental adenosine-mediated DNA hypomethylation predominantly occurs in spongiotrophoblasts and labyrinthine trophoblasts and that this effect is independent of A2B adenosine receptor activation in both preeclampsia models. Extending our mouse findings to humans, we used cultured human trophoblasts to demonstrate that adenosine functions intracellularly and induces DNA hypomethylation without A2B adenosine receptor activation. Altogether, both mouse and human studies reveal novel mechanisms underlying placental DNA hypomethylation and potential therapeutic approaches for preeclampsia.
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PMID:Elevated Adenosine Induces Placental DNA Hypomethylation Independent of A2B Receptor Signaling in Preeclampsia. 2850 74