NITROFURANTOIN-STIMULATED REACTIVE OXYGEN SPECIES PRODUCTION AND GENOTOXICITY IN DIGESTIVE GLAND MICROSOMES AND CYTOSOL OF THE COMMON MUSSEL (MYTILUS-EDULIS-L)
NITROFURANTOIN-STIMULATED REACTIVE OXYGEN SPECIES PRODUCTION AND GENOTOXICITY IN DIGESTIVE GLAND MICROSOMES AND CYTOSOL OF THE COMMON MUSSEL (MYTILUS-EDULIS-L)
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DOI：
10.1006/taap.1995.1076
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发表时间：
1995-04-01
影响因子：
3.8
通讯作者：
LIVINGSTONE, DR
中科院分区：
文献类型：
--
作者：
MARTINEZ, PG;WINSTON, GW;LIVINGSTONE, DR
以紫贻贝（Mytilus edulis）消化腺亚细胞组分为材料，研究了呋喃妥因（NF）产生活性氧（ROS）的能力。H2 O2（过氧化氢酶的作用）和羟基自由基（（OH）-O-.）(iron/EDTA介导的KMBA氧化成乙烯）。此外，使用鼠伤寒沙门氏菌umu致突变试验检查NF的遗传毒性效应。NF刺激微粒体NAD（P）H依赖性氧消耗，导致H2 O2形成。NF刺激微粒体O-2（-）的产生对于NADH是明显的，但对于NADPH不是，至少证实了前者辅酶的氧化还原循环。两种辅酶对胞质组分的O-2（-）产生无明显刺激作用。NF刺激微粒体NAD（P）H依赖性（OH）-O-。生产;（OH）-O-的速率。NADH的产量大于NADPH;和（OH）-O-。表明至少部分地通过铁催化的Haber-Weiss反应形成。一个角色被指示为自由基驱动的芬顿反应在NF-刺激的微粒体生产（OH）-O-。从NADPH在细胞质中观察到NF产生的致突变物质，但在微粒体中未观察到，前者对NADH的影响大于NADPH。总体而言，认为NAD（P）H依赖性微粒体产生ROS以及ROS产生与致突变性缺乏相关性表明消化腺通过单电子和双电子还原途径代谢NF的潜力。从这项研究和其他研究，增强活性氧生产NF和其他氧化还原循环外源性物质是一种普遍的现象，在水生生物和污染物介导的毒性的潜在机制。(C)出版社：Academic Press
The ability of nitrofurantoin (NF) to produce reactive oxygen species (ROS) was investigated in subcellular fractions of digestive gland of the mussel Mytilus edulis in terms of oxygen consumption and the formation of superoxide anion radical (O-2(-)) (measured as SOD-sensitive cytochrome c reduction or SOD-sensitive (OH)-O-. production), H2O2 (effects of catalase), and hydroxyl radical ((OH)-O-.) (iron/EDTA-mediated oxidation of KMBA to ethylene). Additionally, the genotoxic effects of NF were examined using the Salmonella typhimurium umu mutagenicity assay. Microsomal NAD(P)H-dependent oxygen consumption was stimulated by NF, leading to the formation of H2O2. Stimulation of microsomal O-2(-) production by NF was evident for NADH but not NADPH, confirming redox cycling at least with the former coenzyme. No stimulation of O-2(-) production was obvious for cytosolic fraction with either coenzyme. NF stimulated microsomal NAD(P)H-dependent (OH)-O-. production; the rates of (OH)-O-. production were greater for NADH than NADPH; and the (OH)-O-. was indicated to be formed, at least in part, by an iron-catalyzed Haber-Weiss reaction. A role was indicated for a free radical driven Fenton reaction in the NF-stimulated microsomal production of (OH)-O-. from NADPH. The production of mutagenic species from NF was observed for cytosol but not for microsomes, and the former effects were greater for NADH than NADPH. Overall, the NAD(P)H-dependent microsomal generation of ROS, and the lack of correlation of ROS production with mutagenicity, are considered indicative of the potential of digestive gland to metabolize NF by both one-electron and two-electron reductive pathways. From this and other studies, enhanced ROS production by NF and other redox cycling xenobiotics is indicated to be a widespread phenomenon in aquatic organisms and a potential mechanism of pollutant-mediated toxicity. (C) 1995 Academic Press,Inc.