Abstract
Nitric oxide (NO) has been reported to function in both cytoprotective and cytotoxic tissue ischemia-reperfusion (I/R). In this study, we evaluated the effects of L-arginine, the substrate for NO, and NG-nitro L-arginine methyl ester (L-NAME), NO synthase (NOS) inhibitor on super--oxide dismutase (SOD) enzyme activity, malondialdehyde (MDA), a marker of lipid peroxidation, nitrate levels, and histopathological structure in rat sciatic nerve 2 h after ischemia, followed by 3 h of reperfusion. Reperfusion resulted in a significant increase in lipid peroxidation level and a decrease in nitrate level of the sciatic nerve. The increased level of lipid peroxidation was partly reduced by NOS inhibition. The decrease in sciatic nerve SOD level, observed in group subjected to I/R, was prevented by inhibition of NOS by L-NAME. These results were supported by histological findings that in the L-arginine-treated group, degenerations of both myelin sheath and axon were observed, while in the L--NAME-treated group, no pathological changes were detected. Our results suggested that excessive NO formation accelerates lipid peroxidation, as well as axonal degeneration on the early reperfusion period of the sciatic nerve
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
