酗酒者红细胞δ-氨基-γ-酮戊酸脱水酶活性降低。 - Suppr

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超能文献

Depression of erythrocyte delta-aminolaevulinic acid dehydratase activity in alcoholics.

作者信息

Krasner N, Moore M R, Thompson G G, McIntosh W, Goldberg A

出版信息

Clin Sci Mol Med. 1974 Mar;46(3):415-8. doi: 10.1042/cs0460415.

DOI:10.1042/cs0460415

PMID:4150433

Abstract

摘要

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引用本文的文献

[Hepatic porphyrias and alcohol].[肝性卟啉病与酒精]

Med Klin (Munich). 1999 Jun 15;94(6):314-28. doi: 10.1007/BF03044890.

The action of small doses of lead on erythrocyte D-aminolevulinic acid dehydratase in the mouse.小剂量铅对小鼠红细胞δ-氨基乙酰丙酸脱水酶的作用

Arch Toxicol. 1980 Jan;43(3):213-20. doi: 10.1007/BF00297586.

The in vivo effects of zinc on erythrocyte delta-aminolaevulinic acid dehydratase in man.

Int Arch Occup Environ Health. 1980 Feb;45(2):163-8. doi: 10.1007/BF01274135.

The relevance of arguments for excluding ALAD from the recommended biological limit values in occupational exposure to inorganic lead (WHO 1980).关于将δ-氨基-γ-酮戊酸脱水酶排除在职业性接触无机铅的推荐生物限值之外的论据的相关性（世界卫生组织，1980年）

Int Arch Occup Environ Health. 1982;50(4):397-412. doi: 10.1007/BF00377836.

Persistent protoporphyrinemia in hereditary porphobilinogen synthase (delta-aminolevulinic acid dehydrase) deficiency under low lead exposure. A new molecular basis for the pathogenesis of lead intoxication.低铅暴露下遗传性胆色素原合酶（δ-氨基-γ-酮戊酸脱水酶）缺乏所致的持续性原卟啉血症。铅中毒发病机制的一种新分子基础。

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Acute lead poisoning in inherited porphobilinogen synthase (delta-aminolevulinic acid dehydrase) deficiency.遗传性胆色素原合酶（δ-氨基乙酰丙酸脱水酶）缺乏症中的急性铅中毒

Blut. 1982 Aug;45(2):131-9. doi: 10.1007/BF00319941.

Porphobilinogen-synthase (delta-aminolevulinic acid dehydratase) deficiency in bone marrow cells of two patients with porphobilinogen-synthase defect acute porphyria.

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Elevated levels of blood lead in alcoholic liver disease.

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