锰对柠檬酸亚铁在体内诱导的脂质过氧化和黑质纹状体神经变性的新型保护作用。

Novel protective effect of manganese against ferrous citrate-induced lipid peroxidation and nigrostriatal neurodegeneration in vivo.

作者信息

Sziráki I, Rauhala P, Chiueh C C

机构信息

Unit on Neurotoxicology and Neuroprotection, NIMH, Bethesda, MD 20892-1264, USA.

出版信息

Brain Res. 1995 Nov 6;698(1-2):285-7. doi: 10.1016/0006-8993(95)01056-2.

DOI:10.1016/0006-8993(95)01056-2

PMID:8581499

Abstract

Earlier studies intranigrally infusing high doses of manganese (50-250 nmol) revealed a reversible oxidative injury to nigrostriatal dopaminergic neurons. In fact, intranigral infusion of lower dose manganese (4.2 nmol) in the present study did not significantly alter dopamine levels in rat striatum. Moreover, manganese completely suppressed both acute lipid peroxidation in substantia nigra and chronic degeneration of the nigrostriatal neurons induced by intranigral infusion of ferrous citrate (4.2 nmol). These in vivo data indicate that low dose manganese is a potent antioxidant which may activate antioxidative defense mechanisms to protect brain neurons against oxidative stress induced by iron complexes.

摘要

早期研究通过向黑质内注射高剂量锰（50 - 250纳摩尔）发现，黑质纹状体多巴胺能神经元会受到可逆性氧化损伤。事实上，在本研究中向黑质内注射较低剂量的锰（4.2纳摩尔）并未显著改变大鼠纹状体中的多巴胺水平。此外，锰完全抑制了黑质中的急性脂质过氧化以及由向黑质内注射柠檬酸亚铁（4.2纳摩尔）所诱导的黑质纹状体神经元的慢性变性。这些体内实验数据表明，低剂量锰是一种有效的抗氧化剂，它可能激活抗氧化防御机制，以保护脑神经元免受铁复合物诱导的氧化应激的影响。