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铁诱导的氧化应激和线粒体功能障碍:与帕金森病的相关性。

Iron induced oxidative stress and mitochondrial dysfunction: relevance to Parkinson's disease.

作者信息

Harley A, Cooper J M, Schapira A H

机构信息

Department of Neurological Science, Royal Free Hospital School of Medicine, London, UK.

出版信息

Brain Res. 1993 Nov 12;627(2):349-53. doi: 10.1016/0006-8993(93)90341-j.

DOI:10.1016/0006-8993(93)90341-j
PMID:8298979
Abstract

Inactivation of the mitochondrial respiratory chain in response to iron-induced oxidative stress has been studied in cultured cells. Iron loading resulted in malonaldehyde production, decreased levels of glutathione and reduced specific activities of both complexes I and IV of the respiratory chain. These results are discussed with respect to idiopathic Parkinson's disease, which is associated with increased iron levels and a specific decrease in complex I activity in the substantia nigra.

摘要

针对铁诱导的氧化应激反应,对培养细胞中线粒体呼吸链的失活进行了研究。铁负荷导致丙二醛生成、谷胱甘肽水平降低以及呼吸链复合体I和复合体IV的比活性降低。结合特发性帕金森病对这些结果进行了讨论,该病与铁水平升高及黑质中复合体I活性的特异性降低有关。

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Iron induced oxidative stress and mitochondrial dysfunction: relevance to Parkinson's disease.铁诱导的氧化应激和线粒体功能障碍:与帕金森病的相关性。
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