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Effects of sulfhydryl inhibition on red blood cells. I. Mechanism of hemolysis.巯基抑制对红细胞的影响。I. 溶血机制。
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METAL CHELATES OF SOME SULFUR-CONTAINING AMINO ACIDS.某些含硫氨基酸的金属螯合物
Biochemistry. 1964 Jun;3:745-50. doi: 10.1021/bi00894a001.
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STUDIES ON METAL COMPLEXES OF DRUGS; D-PENICILLAMINE AND N-ACETYL-D-PENICILLAMINE.药物金属配合物的研究;D-青霉胺和N-乙酰-D-青霉胺
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PURIFICATION AND PROPERTIES OF GLUTATHIONE REDUCTASE OF HUMAN ERYTHROCYTES.人红细胞谷胱甘肽还原酶的纯化及性质
J Biol Chem. 1963 Dec;238:3928-33.
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[Behavior of glutathione, the glutathione stability test and glucose-6-phosphate dehydrogenase activity in lead poisoning].[铅中毒时谷胱甘肽的行为、谷胱甘肽稳定性试验及葡萄糖-6-磷酸脱氢酶活性]
Minerva Med. 1963 Apr 4;54:930-2.
6
Improved method for the determination of blood glutathione.测定血液中谷胱甘肽的改进方法。
J Lab Clin Med. 1963 May;61:882-8.
7
In vitro pyrrole and porphyrin synthesis in lead poisoning and iron deficiency.铅中毒和缺铁时的体外吡咯和卟啉合成
J Clin Invest. 1963 Jun;42(6):830-9. doi: 10.1172/JCI104775.
8
[Diagnostic value of the determination of the blood glutathione level in chronic lead poisoning in human subjects].[人体慢性铅中毒时血液谷胱甘肽水平测定的诊断价值]
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9
Pbrphyrin biosynthesis in erythrocytes. II. Enzymes converting gamma-aminolevulinic acid to coproporphyrinogen.红细胞中的卟啉生物合成。II. 将γ-氨基乙酰丙酸转化为粪卟啉原的酶。
J Biol Chem. 1958 Jun;232(2):1119-40.
10
On the mode of action of x-ray protective agents. III. The enzymatic reduction of disulfides.关于X射线防护剂的作用方式。III. 二硫化物的酶促还原
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无机铅和镉对人红细胞中谷胱甘肽还原酶系统及δ-氨基乙酰丙酸脱水酶的体内效应比较。

Comparison of in vivo effect of inorganic lead and cadmium on glutathione reductase system and delta-aminolevulinate dehydratase in human erythrocytes.

作者信息

Roels H A, Buchet J P, Lauwerys R R, Sonnet J

出版信息

Br J Ind Med. 1975 Aug;32(3):181-92. doi: 10.1136/oem.32.3.181.

DOI:10.1136/oem.32.3.181
PMID:1156566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1008057/
Abstract

The activity of delta-aminolevulinate dehydratase (ALAD) of erythrocytes, the lead (Pb-B) and cadmium (Cd-B) concentration in whole blood, the content of reduced glutathion (GSH) in erythrocytes, and the regeneration rate of GSH by intact erythrocytes were measured during an epidemiological survey of 84 men employed in a Belgian cadmium and lead producing plant. A control group of 26 persons (students and laboratory staff) was also examined. The logarithm of the ALAD activity is highly inversely correlated with log Pb-B (r = -0.760) but no correlation was found with log Cd-B. There exists a significant negative correlation between GSH and log Pb-B (r = -0.423) but not between GSH AND LOG Cd-B. The apparently good relationship between log ALAD and GSH disappeared completely by holding log Pb-B constant, but log ALAD remained highly inversely correlated with log Pb-B when standardized for GSH concentration (r = -0.748). In vivo investigation of the GSH regeneration rate of intact erythrocytes demonstrated clearly that the overall activity of the glutathione oxidation-reduction pathways is not impaired in Pb and Cd-exposed workers with significantly increased Pb-B and Cd-B, since their initial GSH regeneration rate (first 15 minutes) was identical with that of the control group. Results of similar in vitro experiments in which control whole blood was incubated before-hand with Pb2+ or Cd2+, or both, reinforce this conclusion. Since increased Cd-B and Pb-B do not influence the glutathione reductase system of erythrocytes, and since endogenous erythrocyte GSH is not correlated with Cd-B, the moderate decrease in endogenous erythrocyte Gsh found in Pb-exposed workers might result from a Pb-induced impairment for the erythrocyte mechanism for glutathione synthesis.

摘要

在对一家比利时镉铅生产厂的84名男性员工进行的流行病学调查中,测量了红细胞δ-氨基乙酰丙酸脱水酶(ALAD)的活性、全血中铅(Pb-B)和镉(Cd-B)的浓度、红细胞中还原型谷胱甘肽(GSH)的含量以及完整红细胞中GSH的再生率。还对26名对照组人员(学生和实验室工作人员)进行了检查。ALAD活性的对数与log Pb-B高度负相关(r = -0.760),但与log Cd-B未发现相关性。GSH与log Pb-B之间存在显著负相关(r = -0.423),但与log Cd-B之间不存在相关性。通过保持log Pb-B不变,log ALAD与GSH之间明显的良好关系完全消失,但当以GSH浓度标准化时,log ALAD与log Pb-B仍高度负相关(r = -0.748)。对完整红细胞GSH再生率的体内研究清楚地表明,在Pb和Cd暴露工人中,尽管他们的Pb-B和Cd-B显著增加,但谷胱甘肽氧化还原途径的整体活性并未受损,因为他们最初的GSH再生率(最初15分钟)与对照组相同。在体外进行的类似实验结果,即事先将对照全血与Pb2+或Cd2+或两者一起孵育,进一步证实了这一结论。由于Cd-B和Pb-B的增加不影响红细胞的谷胱甘肽还原酶系统,并且由于内源性红细胞GSH与Cd-B不相关,因此在Pb暴露工人中发现的内源性红细胞Gsh适度下降可能是由于Pb诱导的红细胞谷胱甘肽合成机制受损所致。