Why the study?
The interactions of paraoxonase 1 with nitric oxide synthase, nitric oxide, and derived reactive species needed to be determined, especially regarding their pathological implications.
Key points are not available for this paper at this time.
Design
Review
May prompt mechanistic research on vascular oxidative stress; leaves open clinical translation of paraoxonase 1-nitric oxide interactions.
One of the best consolidated paradigms in vascular pharmacology is that an uncontrolled excess of oxidizing chemical species causes tissue damage and loss of function in the endothelial and subendothelial layers. The fact that high-density lipoproteins play an important role in preventing such an imbalance is integrated into that concept, for which the expression and activity of paraoxonases is certainly crucial. The term paraoxonase (aryldialkyl phosphatase, EC 3.1.8.1) encompasses at least three distinct isoforms, with a wide variation in substrate affinity, cell and fluid localization, and biased expression of polymorphism. The purpose of this review is to determine the interactions that paraoxonase 1 has with nitric oxide synthase, its reaction product, nitric oxide (nitrogen monoxide, NO), and its derived reactive species generated in an oxidative medium, with a special focus on its pathological implications.
No takes yet. Share an insight, caveat, or question.
Marín et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: