Ovid.com  |  Login  |  Technical Support  
ovid_logo
Search:

Advanced Search
Ovid News
Learn about Ovid’s new research content and products.
Ovid Events
Check out where Ovid is across the globe at industry conferences and events worldwide.
Are you affiliated with a leading medical or academic institution?
If so, send your librarian an email recommending titles you’ve found valuable for research at your institution.
Home About Products & Services Contact Us btn_contact1
Clinical Chemistry and Laboratory Medicine
tabmenu

March 2008, 46:3 > Increased plasma asymmetric dimethylarginine...
< Previous  |   Next >
ARTICLE LINKS:
Fulltext  |  PDF (98 K)
Increased plasma asymmetric dimethylarginine (ADMA) levels in retinal venous occlusive disease.

Article

Clinical Chemistry & Laboratory Medicine. 46(3):387-392, March 2008.
Zinellu, Angelo 1,2,*; Pinna, Antonio 3; Sotgia, Salvatore 1,2; Zinellu, Elisabetta 4; Usai, Maria Franca 1; Carta, Francesco 3; Gaspa, Leonardo 1,2; Deiana, Luca 1; Carru, Ciriaco 1,2,*

Abstract:
Background: We investigated the levels of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA), as well as homocysteine and cysteine thiols, in a cohort of subjects affected by retinal vein occlusion (RVO) disease.

Methods: Capillary electrophoresis analysis was performed in both RVO subjects (ns54) and in a control group (n s 32).

Results: No differences were found between controls and patients; however, after categorisation for RVO type, central RVO (CRVO) patients showed higher levels of ADMA (0.710 +/- 0.139 [mu]mol/L) than controls (0.635 +/- 0.117 [mu]mol/L) and branch RVO patients (0.642 +/- 0.096 [mu]mol/L). Moreover, cysteine plasma levels were also significantly higher in CRVO patients than in controls (265.8 +/- 46.9 vs. 226.7 +/- 51.9 [mu]mol/L, p-0.01), while homocysteine plasma concentration was more or less identical in all groups.

Conclusions: We hypothesise that the elevated levels of cysteine in CRVO patients may post-translationally inhibit dimethylarginine dimethylaminohydrolase enzyme activity, as already described for homocysteine, thus contributing to the accumulation of ADMA in this patient group.

Copyright (C) 2008 Walter de Gruyter