Spintrapping of nitric oxide

Nitric oxide is the driving force behind oxidative stress. To elucidate its origins and mechanisms may help reducing oxidative stress.

Introduction

(Muller et al. 2003)

Sodium nitroprusside and low-molecular weight S-nitrosothiols are some of the nitric oxide (NO) donors that cause vasodilatation, which means that effected arteries cannot contract. Circulation will decelerate. It may even collapse. Medicinal studies from the late 1990s identified oxidative stress as the main cause. At the same time the question arose if the NO free radical really is the main culprit. In fact, nitrosation of cystein‘s sulphydryl group is more likely to have a longterm effect.

 

Advantages of Colloid Fe(II)-Diethyldithiocarbamate (Fe(II)(DETC)2)

  • high efficiency of nitric oxide spin trapping

  • basal as well as stimulated nitric oxide production can be quantified in aorta and vena cava

  • colloid Fe(II)(DETC)2 is lipophilic and “water-soluble”

  • Cu(DETC)2-signal doesn't dominate over the NO- Fe(II)(DETC)2Signal

  • no inhibition of vascular SOD activity

  • nitric oxide detection is not affected by moderately increased levels of extracellular superoxide and nitrite.

 

Results

(Muller et al. 2003)

NO-donors were tested in their ability to contradict norepinephrine (NE), which causes artery contraction. To keep results independent from animal species, observation went down in porcine coronary arteries as well as rat aorta. Two categories of NO-donors have been found:

1) NE deactivating species, such as GSNO, SNAP, SNAC & SNP, cause NE to respond significantly less

2) not NE affecting species, such as  DEA-NO, SIN-1, GTN & CysNO, which did inhibit artery contraction

 

 

References