Nitrosyl complex formation during endotoxin-induced injury in the rat small intestine.
Nitrosyl complex formation during endotoxin-induced injury in the rat small intestine.
复制标题
内毒素诱导的大鼠小肠损伤过程中亚硝酰复合物的形成。
作者：
W. Chamulitrat;N. Skrepnik;J. Spitzer
本研究的目的是证明一氧化氮（NO）的生产，并确定其在大鼠小肠内毒素治疗后的作用。通过使用电子顺磁共振（EPR）光谱，我们能够检测到高浓度的亚硝基化蛋白质在小肠的大鼠给予1毫克/千克脂多糖（LPS），并在6小时后处死。非血红素和血红素亚硝酰复合物的EPR谱在上皮层和肠壁中被检测到。在这些大鼠的管腔内容物中仅检测到亚硝基血红素蛋白复合物的EPR谱特征。脂多糖管理升高浓度的肠道脂质过氧化生物标志物，硫代巴比妥酸反应物质，共轭二烯。NO合酶抑制剂处理可减弱这些变化。我们的结论是与NO形成相关的氧化剂至少部分参与组织脂质的氧化。这一过程可能是LPS致肠损伤的机制之一。
The objective of this study was to demonstrate nitric oxide (NO) production and determine its role in the rat small intestine following endotoxin treatment. By using electron paramagnetic resonance (EPR) spectroscopy, we were able to detect high concentrations of nitrosylated proteins in the small intestines of rats administered 1 mg/kg lipopolysaccharide (LPS) and sacrificed 6 h later. EPR spectra of non-heme and heme nitrosyl complexes were detected in the epithelium layer and intestinal wall. Only EPR spectra characteristic of nitrosyl hemoprotein complexes were detected in the luminal contents of these rats. LPS administration elevated the concentrations of intestinal lipid peroxidation biomarkers, thiobarbituric acid-reactive substances, and conjugated dienes. These changes were attenuated by NO synthase inhibitor treatment. We conclude that oxidants associated with NO formation were at least in part involved in the oxidation of tissue lipids. This process may be one of the mechanisms of intestinal injury induced by LPS.