S-亚硝基硫醇和一氧化氮，而非硝普钠，在体内可保护黑质纹状体多巴胺能神经元免受铁诱导的氧化应激损伤。
S-nitrosothiols and nitric oxide, but not sodium nitroprusside, protect nigrostriatal dopamine neurons against iron-induced oxidative stress in vivo.
作者信息
Rauhala P, Mohanakumar K P, Sziraki I, Lin A M, Chiueh C C
机构信息
Laboratory of Clinical Science, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-1264, USA.
出版信息
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。
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