CONGENITAL METHEMOGLOBINEMIA WITH A DEFICIENCY OF CYTOCHROME-B5
CONGENITAL METHEMOGLOBINEMIA WITH A DEFICIENCY OF CYTOCHROME-B5
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DOI：
10.1056/nejm198603203141206
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发表时间：
1986-03-20
影响因子：
158.5
通讯作者：
KAFTORY, A
中科院分区：
文献类型：
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作者：
HEGESH, E;HEGESH, J;KAFTORY, A
人们普遍认为，红细胞具有维持血红蛋白处于活性状态的酶还原机制。1,2 还原依赖于还原吡啶核苷酸的再生也已得到充分证实。345 用亚硝酸盐处理红细胞，并将其与葡萄糖、乳酸或其他允许产生还原吡啶核苷酸的底物一起孵育，可促进高铁血红蛋白还原。1,2,6,7在正常条件下，NADH（还原型吡啶核苷酸）会促进高铁血红蛋白还原。烟酰胺腺嘌呤二核苷酸）负责红细胞的大部分高铁血红蛋白还原能力。2,891011NADH 脱氢酶（不同名称为高铁血红蛋白还原酶或细胞色素 b5 还原酶）已被证明是 的组成部分。 。 。
IT is generally accepted that red cells possess enzymatic reducing mechanisms that maintain hemoglobin in its active state.1,2It is also well established that the reduction is dependent on the regeneration of reduced pyridine nucleotides.345Treating red cells with nitrite and incubating them with glucose, lactate, or other substrates that allow the production of reduced pyridine nucleotides promotes methemoglobin reduction.1,2,6,7Under normal conditions, NADH (reduced nicotinamide adenine dinucleotide) accounts for most of the methemoglobin-reducing capacity of the erythrocyte.2,891011An NADH dehydrogenase — variously named methemoglobin reductase or cytochrome b5 reductase — has been proved to be a component of the . . .