亨廷顿舞蹈症中烟酰胺腺嘌呤二核苷酸（NADH）：泛醌氧化还原酶（复合体I）存在缺陷的证据。
Evidence for a defect in NADH: ubiquinone oxidoreductase (complex I) in Huntington's disease.
作者信息
Parker W D, Boyson S J, Luder A S, Parks J K
机构信息
Department of Neurology, University of Colorado School of Medicine, Denver.
出版信息
Neurology. 1990 Aug;40(8):1231-4. doi: 10.1212/wnl.40.8.1231.
We evaluated electron transport chain activity in platelet mitochondria taken from HD patients. All 5 patients studied had striking depressions of NADH:ubiquinone oxidoreductase activity (complex I) (5.36 +/- 2.91 nmol/min/mg; control mean, 19.12 +/- 5.64 nmol/min/mg). Other electron transport chain activities were not significantly different from control values. HD may be caused by a mutation in 1 of the nuclear coded subunits of NADH:ubiquinone oxidoreductase.
我们评估了来自HD患者的血小板线粒体中的电子传递链活性。所有5名接受研究的患者的NADH：泛醌氧化还原酶活性（复合体I）均显著降低（5.36±2.91 nmol/分钟/毫克；对照组平均值为19.12±5.64 nmol/分钟/毫克）。其他电子传递链活性与对照值无显著差异。HD可能是由NADH：泛醌氧化还原酶的一个核编码亚基发生突变引起的。
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