کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9879403 | 1534757 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Enzymes that hydrolyze adenine nucleotides in chronic renal failure: Relationship between hemostatic defects and renal failure severity
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
The activities of the enzymes NTPDase (E.C.3.6.1.5, apyrase, ATP diphosphohydrolase, ecto-CD39) and 5â²-nucleotidase (E.C.3.1.3.5, CD73) were analyzed in platelets from patients with chronic renal failure (CRF), both undergoing hemodialysis treatment (HD) and not undergoing hemodialysis (ND), as well as from a control group. The results showed an increase in platelet NTPDase activity in CRF patients on HD treatment (52.88%) with ATP as substrate (PÂ <Â 0.0001). ADP hydrolysis was decreased (33.68% and 39.75%) in HD and ND patients, respectively. In addition, 5â²-nucleotidase activity was elevated in the HD (160%) and ND (81.49%) groups when compared to the control (PÂ <Â 0.0001). Significant correlation was found among ATP, ADP and AMP hydrolysis and plasma creatinine and urea levels (PÂ <Â 0.0001). Patients were compared statistically according the time of hemodialysis treatment. We found enhanced NTPDase and 5â²-nucleotidase activities between 49 and 72 months on HD patients. Our result suggests the existence of alterations in nucleotide hydrolysis in platelets of CRF patients. Possibly, this altered nucleotide hydrolysis could contribute to hemostasis abnormalities found in CRF.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1741, Issue 3, 25 September 2005, Pages 282-288
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1741, Issue 3, 25 September 2005, Pages 282-288
نویسندگان
Adriane C. Silva, André L.B. Morsch, Rafael F. Zanin, MaÃsa C. Corrêa, LuÃs C. Arantes, Maria C. Araujo, Vera M. Morsch, Maria R.C. Schetinger,