Rauhala P, Mohanakumar K P, Sziraki I, Lin A M, Chiueh C C
Laboratory of Clinical Science, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-1264, USA.
Synapse. 1996 May;23(1):58-60. doi: 10.1002/(SICI)1098-2396(199605)23:1<58::AID-SYN7>3.0.CO;2-G.
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-nitrosoglutathione (GSNO) and S-nitroso-N-acetylpenicillamine (SNAP) or nitric oxide (approximately 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.
向大鼠黑质纹状体系统的黑质内注入柠檬酸亚铁（4.2纳摩尔）会在黑质中引发急性脂质过氧化，并在纹状体中导致慢性多巴胺耗竭。共同注入8.4纳摩尔的一氧化氮供体，如S-亚硝基谷胱甘肽（GSNO）和S-亚硝基-N-乙酰青霉胺（SNAP）或一氧化氮（约2纳摩尔），可保护黑质纹状体神经元免受铁诱导的脂质过氧化及相关氧化损伤。然而，硝普钠（SNP，8.4纳摩尔）会加剧柠檬酸亚铁引起的多巴胺耗竭，因为SNP是一种铁氰化物复合物。目前的体内实验结果表明，一氧化氮和S-亚硝基硫醇是抗氧化剂，可保护脑多巴胺能神经元免受氧化应激/损伤。
