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A computational model for biochemical Interaction of NO and reactive oxygen species in paired arteriole‐venule
Author(s) -
Kavdia Mahendra
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.747.14
Subject(s) - peroxynitrite , superoxide , oxidative stress , reactive oxygen species , venule , arteriole , chemistry , antioxidant , microbiology and biotechnology , biochemistry , biophysics , vascular smooth muscle , oxidative phosphorylation , endothelium , biology , endocrinology , enzyme , circulatory system , smooth muscle
All cells of vascular tissue including endothelial cells, and smooth muscle cells have enzyme systems that produce reactive oxygen species (ROS). Important ROS generated in the vascular tissue are superoxide or hydrogen peroxide. Superoxide can react with NO to form peroxynitrite. Antioxidant systems protect against damage from ROS in normal physiological conditions. When ROS generation overwhelms the antioxidant defense (known as oxidative stress), these radicals can alter cellular function by interacting with DNA, RNA, and fatty acids, contribute to impairment of endothelium‐dependent vasodilation and lead to apoptosis. In this study, a computational model to describe the interactions of NO, superoxide and peroxynitrite in a tissue containing an arteriole/venule pair is presented. We simulated two sources of oxidative stress 1) NADPH oxidases and 2) adhered/migrated leukocytes. Model results predicted that 1) an increase in oxidative stress in the venule decreased NO levels in regions of both venule and neighboring arteriole, and 2) the amount of NO reduction varied depending on the location of oxidative. The results provide a comprehensive quantitative knowledge of NO and ROS interactions in vascular tissue, which is an important step towards understanding vascular complications in many pathological conditions.