Nitric oxide, oxidative stress, and progression of chronic renal failure
PS Modlinger, CS Wilcox, S Aslam - Seminars in nephrology, 2004 - Elsevier
Cellular injury or organ dysfunction from oxidative stress occurs when reactive oxygen
species (ROS) accumulate in excess of the host defense mechanisms. The deleterious effect
of ROS occurs from 2 principal actions. First, ROS can inactivate mitochondrial enzymes,
damage DNA, or lead to apoptosis or cellular hypertrophy. Second, nitric oxide (NO), which
is a principal endothelial-derived relaxing factor, reacts with superoxide anion (O2−) to yield
peroxynitrite (ONOO−), which is a powerful oxidant and nitrosating agent. The inactivation of …
species (ROS) accumulate in excess of the host defense mechanisms. The deleterious effect
of ROS occurs from 2 principal actions. First, ROS can inactivate mitochondrial enzymes,
damage DNA, or lead to apoptosis or cellular hypertrophy. Second, nitric oxide (NO), which
is a principal endothelial-derived relaxing factor, reacts with superoxide anion (O2−) to yield
peroxynitrite (ONOO−), which is a powerful oxidant and nitrosating agent. The inactivation of …