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职业性铅暴露对血红素生物合成中淋巴细胞酶的影响。

Effect of occupational lead exposure on lymphocyte enzymes involved in heme biosynthesis.

作者信息

Rossi E, Costin K A, Garcia-Webb P

机构信息

Department of Clinical Biochemistry, Queen Elizabeth II Medical Centre, Nedlands, Western Australia.

出版信息

Clin Chem. 1990 Nov;36(11):1980-3.

PMID:2242583
Abstract

Lead exposure is a well-known cause of increases in urinary coproporphyrin and erythrocyte zinc-protoporphyrin, so these compounds are often used to monitor occupational lead exposure. The increased concentrations are usually assumed to result from lead inhibition of two of the mitochondrial enzymes of heme biosynthesis, coproporphyrinogen oxidase (EC 1.3.3.3) and ferrochelatase (EC 4.99.1.1). We studied 88 subjects in whom the degree of occupational lead exposure was established by measuring erythrocyte lead and protoporphyrin. Assay of lymphocyte coproporphyrinogen oxidase and ferrochelatase activities showed that these enzymes were unaffected by lead exposure, as was a related enzyme, lymphocyte NADH-ferricyanide reductase. We propose alternative explanations for the increased concentrations of coproporphyrin and zinc-protoporphyrin seen in lead exposure.

摘要

铅暴露是导致尿中粪卟啉和红细胞锌原卟啉升高的一个众所周知的原因,因此这些化合物常被用于监测职业性铅暴露。浓度升高通常被认为是由于铅抑制了血红素生物合成的两种线粒体酶,即粪卟啉原氧化酶(EC 1.3.3.3)和亚铁螯合酶(EC 4.99.1.1)。我们研究了88名通过测量红细胞铅和原卟啉来确定职业性铅暴露程度的受试者。淋巴细胞粪卟啉原氧化酶和亚铁螯合酶活性的测定表明,这些酶不受铅暴露的影响,一种相关酶,淋巴细胞NADH-铁氰化物还原酶也是如此。我们对铅暴露时所见的粪卟啉和锌原卟啉浓度升高提出了其他解释。

相似文献

1
Effect of occupational lead exposure on lymphocyte enzymes involved in heme biosynthesis.职业性铅暴露对血红素生物合成中淋巴细胞酶的影响。
Clin Chem. 1990 Nov;36(11):1980-3.
2
Lead and the terminal mitochondrial enzymes of haem biosynthesis.铅与血红素生物合成的终末线粒体酶
Biomed Chromatogr. 1993 Jan-Feb;7(1):1-6. doi: 10.1002/bmc.1130070102.
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Lead toxicity and heme biosynthesis.铅中毒与血红素生物合成
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4
Multiple mechanisms for the regulation of haem synthesis during erythroid cell differentiation. Possible role for coproporphyrinogen oxidase.红细胞分化过程中血红素合成调控的多种机制。粪卟啉原氧化酶的可能作用。
Biochem J. 1991 Apr 15;275 ( Pt 2)(Pt 2):321-6. doi: 10.1042/bj2750321.
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In situ conversion of coproporphyrinogen to heme by murine mitochondria: terminal steps of the heme biosynthetic pathway.小鼠线粒体将粪卟啉原原位转化为血红素:血红素生物合成途径的终端步骤。
Protein Sci. 1993 Jul;2(7):1092-8. doi: 10.1002/pro.5560020703.
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History and background of protoporphyrin testing.
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Zinc chelatase in human lymphocytes: detection of the enzymatic defect in erythropoietic protoporphyria.人淋巴细胞中的锌螯合酶:红细胞生成性原卟啉症中酶缺陷的检测
Anal Biochem. 1988 Oct;174(1):146-50. doi: 10.1016/0003-2697(88)90529-5.
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Formation of zinc protoporphyrin in cultured hepatocytes: effects of ferrochelatase inhibition, iron chelation or lead.培养肝细胞中锌原卟啉的形成:亚铁螯合酶抑制、铁螯合或铅的影响
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Effects of iron deficiency and chronic iron overloading on mitochondrial heme biosynthetic enzymes in rat liver.缺铁和慢性铁过载对大鼠肝脏线粒体血红素生物合成酶的影响。
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引用本文的文献

1
Environmental chemical exposures and disturbances of heme synthesis.环境化学物质暴露与血红素合成紊乱
Environ Health Perspect. 1997 Feb;105 Suppl 1(Suppl 1):37-53. doi: 10.1289/ehp.97105s137.
2
Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development.发育过程中正常和缺铁大鼠体内铅与铁的组织摄取之间的相互作用。
Biol Trace Elem Res. 1996 Jun;52(3):249-61. doi: 10.1007/BF02789166.