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S‐nitrosothiols and nitric oxide, but not sodium nitroprusside, protect nigrostriatal dopamine neurons against iron‐induced oxidative stress in vivo
Author(s) -
Rauhala Pekka,
Mohanakumar K. Parameswarannay,
Sziraki Istvan,
Lin Anya M.Y.,
Chiueh Chuang C.
Publication year - 1996
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199605)23:1<58::aid-syn7>3.0.co;2-g
Subject(s) - sodium nitroprusside , nitric oxide , dopamine , oxidative stress , chemistry , in vivo , pharmacology , nitrosylation , neuroscience , biophysics , biochemistry , medicine , biology , organic chemistry , microbiology and biotechnology
Intranigral infusion of ferrous citrate (4.2 nmol) induced an acute lipid peroxidation in the substantia nigra and a chronic dopamine depletion in the striatum of rat nigrostriatal system. Coinfusion of 8.4 nmol nitric oxide donors such as S ‐nitroso‐glutathione (GSNO) and S ‐nitroso‐ N ‐acetylpenicillamine (SNAP) or nitric oxide (∼2 nmol) protected nigrostriatal neurons against iron‐induced lipid peroxidation and associated oxidative injury. However, sodium nitroprusside (SNP, 8.4 nmol) augmented dopamine depletion caused by ferrous citrate because SNP is a ferricyanide complex. The present in vivo results indicate that nitric oxide and S ‐nitrosothiols are antioxidants which can protect brain dopamine neurons against oxidant stress/damage. © 1996 Wiley‐Liss, Inc.