Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion.
First-pass extracted concept
peroxynitrite
Evidence Snippets
Supporting Sources
Linked Claims
Peroxynitrite-driven reactions can modulate signaling or cause overwhelming oxidative injury leading to necrosis or apoptosis.
These reactions trigger cellular responses ranging from subtle modulations of cell signaling to overwhelming oxidative injury, committing cells to necrosis or apoptosis.
In vivo peroxynitrite generation is presented as a crucial pathogenic mechanism across multiple diseases including stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders.
In vivo, peroxynitrite generation represents a crucial pathogenic mechanism in conditions such as stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders.
The review states that much cytotoxicity previously attributed to nitric oxide is instead due to peroxynitrite formed by reaction of nitric oxide with superoxide.
Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion.
Peroxynitrite reacts with lipids, DNA, and proteins through direct oxidative and indirect radical-mediated mechanisms.
Peroxynitrite interacts with lipids, DNA, and proteins via direct oxidative reactions or via indirect, radical-mediated mechanisms.
The review proposes that pharmacological strategies aimed at removing peroxynitrite may be powerful therapeutic tools.
Hence, novel pharmacological strategies aimed at removing peroxynitrite might represent powerful therapeutic tools in the future.