Iron potentiates nitric oxide scavenging by dithiocarbamates in tissue of septic shock mice

被引：27

作者：

Komarov, AM ^{[1
]}

Mak, IT ^{[1
]}

Weglicki, WB ^{[1
]}

机构：

[1] GEORGE WASHINGTON UNIV, MED CTR, DEPT PHYSIOL, DEPT EXPT MED, WASHINGTON, DC 20037 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 1997年 / 1361卷 / 03期

关键词：

spin trapping; EPR; nitric oxide; mononitrosyl iron complex; septic shock; (mouse);

D O I：

10.1016/S0925-4439(97)84636-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Vanin and co-workers (Kubrina et al., Biochim. Biophys, Acta 1176 (1993) 240-244; Mikoyan et al., Biochim. Biophys. Acta 1269 (1995) 19-24) reported that short term (30 min) iron (Fe) exposure potentiates nitric oxide (NO) production in tissues of septic shock mice, based on increased formation of NO complex by diethyldithiocarbamate (DETC). We have reexamined the effect of Fe administration in mice treated with Escherichia coli lipopolysaccharide (LPS) and have not found any changes in nitrosylhemoglobin (HbNO) or (NO2- + NO3-) levels in blood 30 min after Fe-citrate complex injection. However, Fe-citrate promotes NO complex formation by iron-dependent NO traps: DETC, pyrrolidinedithiocarbamate (PDTC) and N-methyl-D-glucamine dithiocarbamate (MGD), when given simultaneously at 6 h after LPS. Rather than potentiation of NO production, our data support that short-term iron treatment (30 min) enhances in vivo spin trapping ability of dithiocarbamate. (C) 1997 Elsevier Science B.V.

引用

页码：229 / 234

页数：6

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