正常和 G6PD 缺乏条件下氧化应激对 G6PD 活性和 RBC 脆性的同步作用。

Synchrony of G6PD activity and RBC fragility under oxidative stress exerted at normal and G6PD deficiency.

机构信息

Pharmacology Department, Faculty of Medicine, Mutah University, Al-Karak, 61710, Jordan.

出版信息

Clin Biochem. 2010 Mar;43(4-5):455-60. doi: 10.1016/j.clinbiochem.2009.11.007. Epub 2009 Nov 23.

DOI:10.1016/j.clinbiochem.2009.11.007

PMID:19941843

Abstract

OBJECTIVES

To investigative the effects of oxidative stress simultaneously on Glucose-6-phosphate dehydrogenase (G6PD) activity and RBC fragility under normal and G6PD defective conditions.

METHODS

The effects of several nitric oxide (NO) generating compounds and sulfhydryl blocking agents were simultaneously tested in vitro on hemolysate G6PD activities and RBC fragility. These effects were compared between normal subjects and patients with G6PD deficiency.

RESULTS

The NO donor compounds nitrosocysteine, nitrosoarginine and diethylamine caused strong inhibition on normal and defective G6PD activities, while a similar inhibition was observed only at higher concentrations of the sulfhydryl blocking agents: 2-mercaptoethanol , cysteine and reduced glutathione. All these oxidative compounds promoted RBC hemolysis in parallel to their inhibition extents on G6PD activities. The protection of RBC from this hemolysis was achieved by preincubation with NADPH or SNP but not NAD(+) compound.

CONCLUSION

A concomitant response of G6PD activities and RBC fragility towards the oxidative stress was established.

摘要

目的

研究氧化应激对葡萄糖-6-磷酸脱氢酶（G6PD）活性和红细胞脆性的影响，同时在正常和 G6PD 缺陷条件下。

方法

在体外同时测试几种一氧化氮（NO）生成化合物和巯基阻断剂对溶血 G6PD 活性和 RBC 脆性的影响。将这些影响与正常受试者和 G6PD 缺乏症患者进行比较。

结果

NO 供体化合物硝普氨酸、硝基精氨酸和二乙胺对正常和缺陷 G6PD 活性均有强烈抑制作用，而巯基阻断剂 2-巯基乙醇、半胱氨酸和还原型谷胱甘肽仅在较高浓度下观察到类似抑制作用。所有这些氧化化合物都能促进 RBC 溶血，与它们对 G6PD 活性的抑制程度平行。通过用 NADPH 或 SNP 但不是 NAD(+) 化合物预先孵育，可以防止 RBC 发生这种溶血。