Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 10, Issue 22, Pages 2759-2767Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612043383665
Keywords
nitric oxide; nitric oxide synthase; nitric oxide synthase inhibitors; teratogenesis; limb defects; cardiovascular defects; rat; mouse
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Nitric oxide (NO) is generated by a family of NO synthase (NOS) enzymes, including endothelial (eNOS). inducible (iNOS) and neuronal (nNOS). NO is an important bioregulator of a wide variety of physiological processes. Recent experimental evidence indicates that inhibition of NO synthesis can lead to teratogeriesis. The Current review focuses on this aspect of NOS. Exposure of pregnant rodents to non-selective NOS inhibitors, such as N-G-nitro-L-arginine-methyl ester (L-NAME) and N-G-nitro-L-arginine (L-NNA), has been linked to limb reduction defects. The teratogenic phenotype. characterized by hemorrhage and transverse terminal tissue destruction, has been regarded to be compatible with a vascular origin. The critical time for teratogenic response was traced to advanced stages of gestation. Similar limb reduction defects have been described in mice deficient in cNOS. but not in other NOS isoforms. Several observations have led to the proposal that hypoxia and possible consequential generation of reactive oxygen species are involved in the causation of-NOS inhibitors induced limb defects.
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