Nitric oxide scavenging

Nitric oxide scavenging encompasses a range of reactions and pathways by which nitric oxide is chemically inactivated or removed from tissues, primarily via interaction with hemoglobin, myoglobin, mitochondria, and reactive oxygen species (ROS). Hemoglobin within red blood cells is a major site for NO scavenging, with compartmental barriers reducing the reactivity compared to free hemoglobin. Myoglobin and heart mitochondria also contribute significantly to cardiac NO clearance. Additionally, NO reacts with ROS—such as superoxide—producing reactive nitrogen species (RNS) like peroxynitrite, nitrite, and nitrate, which have their own biological signaling functions and toxicities. Cellular NO consumption regulates vascular tone, influences immune defense, and mediates cell death or survival depending on the context and concentrations involved. Dietary antioxidants and drugs can modulate these processes, impacting cardiovascular, immunological, and neurological health.

Other names

NO scavengingnitric oxide consumptionnitric oxide degradation

Drugs may interfere with NO scavenging by: - Donating NO to increase its bioavailability - Inhibiting molecules that scavenge or consume NO (e.g., antioxidants, specific enzyme inhibitors) - Altering redox state to favor NO persistence or destruction