Reactive oxygen species do not cause arsine-induced hemoglobin damage.
Reactive oxygen species do not cause arsine-induced hemoglobin damage.
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活性氧不会引起砷化氢引起的血红蛋白损伤。
DOI：
10.1080/00984109708984002
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Carter,DE
中科院分区：
文献类型：
--
作者：
Hatlelid,KM;Carter,DE
先前的研究表明，砷酸钠- (AsH3-)诱导的血红蛋白（Hb02）损伤可能导致溶血（Hatlelid et al., 1996）。本研究的目的是确定AsH3in溶液、血红蛋白溶液或完整红细胞中是否形成活性氧，如果形成活性氧，则确定这些活性氧是否对观察到的血红蛋白损伤负责。过氧化氢（H202）在含有ash3和hb02或单独含有ash3的水溶液中检测到，但在完整的红细胞或裂解物中检测不到。此外，在hb02和ash3溶液中添加高活性过氧化氢酶（19,200 U/ml）或谷胱甘肽过氧化物酶（68 U/ml），对ash3诱导的损伤只有轻微的保护作用。此外，ash3处理的hb02和h202处理的hbo2的可见光谱差异表明发生了两种不同的降解过程。采用o2依赖性还原法测定了硝基蓝四氮唑（NBT）中超氧阴离子（of）的存在。结果显示Of呈阴性。外源性超氧化物歧化酶（100 ug/ml）对ash3诱导的hb02光谱变化没有影响，羟基自由基清除剂、甘露醇和DMSO（各20 mM）也没有影响。一般抗氧化剂抗坏血酸（<10 mM）和谷胱甘肽（<1 mM）也无影响。上述结果表明，超氧阴离子和羟基自由基（COH）不参与ash3诱导hb02损伤的机制。结果还表明，尽管ash3有助于体外生成h202，但细胞防御足以解毒形成的量。提出了砷作为溶血剂的另一种机制。
Previous work suggested that arsine- (AsH3-) induced hemoglobin (Hb02) damage may lead to hemolysis (Hatlelid et al., 1996). The purpose of the work presented here was to determine whether reactive oxygen species are formed by AsH3in solution, in hemoglobin solutions, or in intact red blood cells, and, if so, to determine whether these species are responsible for the observed hemoglobin damage. Hydrogen peroxide (H202) was detected in aqueous solutions containing AsH3and Hb02or AsH3alone but not in intact red blood cells or lysates. Additionally, high-activity catalase (19,200 U/ml) or glutathione peroxidase (68 U/ml) added to solutions of Hb02and AsH3had only a minor protective effect against AsHyinduced damage. Further, the differences between the visible spectra of AsH3-treated Hb02and H202-treated HbO2indicate that two different degradative processes occur. The presence of superoxide anion (Of) was measured by O2-dependent reduction of nitro blue tetrazolium (NBT). The results were negative for Of. Exogenous superoxide dismutase (100 ug/ml) did not affect AsH3-induced Hb02spectral changes, nor did the hydroxyl radical scavengers, mannitol, and DMSO (20 mM each). The general antioxidants ascorbate (<10 mM) and glutathione (<1 mM) also had no effect. These results indicate that the superoxide anion and the hydroxyl radical COH) are not involved in the mechanism of AsH3-induced Hb02damage. The results also indicate that although AsH3contributes to H202production in vitro, cellular defenses are adequate to detoxify the amount formed. An alternative mechanism by which an arsenic species is the hemolytic agent is proposed.
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氧化血红蛋白变性和红细胞破坏：血红素对红细胞膜的影响。
影响因子：
3.6
作者：
Chiu,D;Lubin,B
通讯作者：
Lubin,B
质膜作为完整人红细胞中道诺霉素氧化还原激活的位点。
影响因子：
5.8
作者：
L. Marcocci;P. Pietrangeli;I. Mavelli;G. Rotilio
通讯作者：
G. Rotilio
砷化氢与血红蛋白的反应。
DOI：
10.1080/009841096161852
发表时间：
1996
期刊：
Journal of toxicology and environmental health
影响因子：
--
作者：
K. Hatlelid;C. Brailsford;D. E. Carter
通讯作者：
D. E. Carter
使用分离的红细胞建立砷化氢毒性的体外模型。
DOI：
10.1006/faat.1995.1066
发表时间：
1995
期刊：
Fundamental and applied toxicology : official journal of the Society of Toxicology
影响因子：
--
作者：
Hatlelid,KM;Brailsford,C;Carter,DE
通讯作者：
Carter,DE