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Exploring the Arginine Methylome by Nuclear Magnetic Resonance Spectroscopy
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Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections

Carmine Zoccali1, Renke Maas, Sebastiano Cutrupi

  • 1CNR-IBIM, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, c/o Ki Point, Gransial SRL, Via Filippini n. 85, 89100 Reggio Calabria, Italy. carmine.zoccali@tin.it

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|December 15, 2006
PubMed
Abstract

Insights

Plasma levels of asymmetrical dimethyl-arginine (ADMA) increase after acute inflammation resolves. This finding suggests that ADMA suppression may stimulate nitric oxide (NO) synthesis during infection recovery.

Area of Science:

  • Biochemistry
  • Physiology
  • Medical Science

Background:

  • Asymmetrical dimethyl-arginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS).
  • ADMA's role in modulating inducible NOS during acute inflammation is under investigation.
  • This study examines ADMA plasma concentrations in patients with acute bacterial infections.

Purpose of the Study:

  • To investigate the changes in plasma ADMA concentration during acute bacterial infections.
  • To compare ADMA levels at the onset of inflammation versus after resolution.
  • To explore the relationship between ADMA, symmetric dimethyl-arginine (SDMA), and inflammatory markers.

Main Methods:

  • Plasma ADMA and SDMA levels were measured in 17 patients with acute bacterial infections.
  • Measurements were taken at the clinical outset of inflammation and after its resolution.
  • Levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin, and nitrotyrosine were assessed.

Main Results:

  • During acute infection, ADMA levels were similar to healthy subjects, while SDMA levels were elevated and correlated with creatinine.
  • Following infection resolution, plasma ADMA increased by 29% (P = 0.01), whereas SDMA remained unchanged.
  • Changes in the ADMA/SDMA ratio suggested inflammatory cytokines might activate ADMA degradation.

Conclusions:

  • Resolution of acute inflammation is associated with increased plasma ADMA concentrations.
  • The findings imply that ADMA suppression might stimulate nitric oxide (NO) synthesis.
  • Plasma ADMA levels may not accurately reflect its inhibitory potential at the cellular level during inflammation resolution.

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