Suramin Selectively Inhibits Inducible Nitric Oxide Synthase at the Calmodulin Binding Site
MetadataShow full item record
Excessive amounts of the free radical nitric oxide (∙NO) can be cytotoxic and has been linked to neurodegenerative pathways involved in several diseases, including Alzheimer’s and Parkinson’s disease. Inhibition of nitric oxide synthase (NOS), the calmodulin (CaM) binding enzyme responsible for ∙NO synthesis (Figure 1), could therefore serve as an effective treatment for some neurodegenerative diseases. NOS exists in three distinct isoforms expressed in respective tissues: endothelial (eNOS) is active in blood vessels and functions in the regulation of blood pressure, neuronal (nNOS) is expressed in nervous tissue where ∙NO is used as a neurotransmitter, and inducible (iNOS) is expressed in immune-active microglial cells where ∙NO is produced in large quantities as a defense mechanism against pathogens. This study focuses on the use of the organic compound suramin for the selective inhibition iNOS, the isoform that's activity has been associated with the aforementioned pathologies.