NO2 DERIVED POLYPEPTIDE ADDUCTS

NO2 衍生的多肽加合物

基本信息

批准号：
2796633
负责人：
Darryl Brice Hood
金额：
$ 10.76万
依托单位：
MEHARRY MEDICAL COLLEGE
依托单位国家：
美国
项目类别：
财政年份：
1994
资助国家：
美国
起止时间：
1994-09-30 至 2001-09-29
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/2796633
关键词：
SDS polyacrylamide gel electrophoresis adduct air pollution autooxidation autoradiography electrospray ionization mass spectrometry environmental toxicology gas chromatography nitrogen oxides nuclear magnetic resonance spectroscopy peptides pollutant interaction protease inhibitor protein sequence unsaturated fatty acids

项目摘要

Lung proteins are obvious targets for reaction with inhaled air pollutants and the project focuses on the molecular mechanisms by which inhaled oxidants may damage polypeptides, in general, and polypeptides vital to the normal structure and function of the lung, specifically. Nitrogen dioxide (NO2) and its associated NO(x) species are examples of atmospheric pollutants derived- from fossil fuel combustion and cigarette smoke. NO2 inhalation toxicological studies in rats have shown that exposure to NO2 produces an "experimental pulmonary emphysema". In vitro NO2 exposures of synthetic decapeptides followed by exposures of recombinant human alpha-1- proteinase inhibitor (which protects the lung from emphysema by inhibiting a neutrophil enzyme) will be performed to determine the susceptibility of these polypeptides to pollutant oxidants. NO2 exposures of the decapeptides, and of inhibitors, followed by exposures of inhibitors and unsaturated hydrocarbons as well as membrane entrapped inhibitors analyzed by Electrospray Ionization Mass Spectrometry, 15N-NMR,13C-15N-NMR,and 1H- NMR and Gas Chromatography will identify specific NO2 derived adducts. These studies will also determine whether the autoxidation of unsaturated fatty acids contributes to polypeptide inactivation; thus diminishing the lung's defenses.

肺蛋白是与吸入空气污染物反应的明显靶标该项目的重点是吸入的分子机制氧化剂通常会损害多肽，而多肽对特别是肺的正常结构和功能。氮二氧化物（NO2）及其相关的NO（X）物种是大气的例子从化石燃料燃烧和香烟烟雾中得出的污染物。 NO2 吸入大鼠的毒理学研究表明，暴露于NO2 产生“实验性肺肺气肿”。体外NO2暴露合成脱肽，然后暴露于重组人α-1- 蛋白酶抑制剂（通过抑制可保护肺免受肺气肿将进行中性粒细胞酶以确定这些对污染物氧化剂的多肽。 NO2暴露脱肽和抑制剂，然后是抑制剂和不饱和碳氢化合物以及被分析的膜抑制剂通过电喷雾电离质谱法，15N-NMR，13C-15N-NMR和1H- NMR和气相色谱法将确定特定的NO2衍生加合物。这些研究还将决定不饱和的自氧化脂肪酸有助于多肽失活；因此减少了肺的防御。

项目成果

期刊论文数量（6）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Malign Asystole During Head-up Tilt Test: A Case Report and Overview.

平视倾斜测试期间恶性心搏停止：病例报告和概述。

DOI：
10.5083/ejcm.20424884.22
发表时间：
2011
期刊：
The European journal of cardiovascular medicine
影响因子：
0
作者：
Islamoglu,Yahya;Cakici,Musa;Alici,Hayri;Davutoglu,Vedat
通讯作者：
Davutoglu,Vedat

Assessment of metabolites and AhR and CYP1A1 mRNA expression subsequent to prenatal exposure to inhaled benzo(a)pyrene.

产前暴露于吸入苯并 (a) 芘后代谢物以及 AhR 和 CYP1A1 mRNA 表达的评估。

DOI：
10.1016/s0736-5748(03)00073-x
发表时间：
2003
期刊：
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
影响因子：
0
作者：
Wu,Jie;Ramesh,Aramandla;Nayyar,Tultul;Hood,DarrylB
通讯作者：
Hood,DarrylB

Environmental contaminant-mixture effects on CNS development, plasticity, and behavior.

DOI：
10.1016/j.taap.2004.01.016
发表时间：
2004-05
期刊：
Toxicology and applied pharmacology
影响因子：
3.8
作者：
D. D. Wormley-D.;A. Ramesh;D. Hood
通讯作者：
D. D. Wormley-D.;A. Ramesh;D. Hood

Inhaled benzo(a)pyrene impairs long-term potentiation in the F1 generation rat dentate gyrus.

DOI：
发表时间：
2004-09
期刊：
Cellular and molecular biology
影响因子：
1.6
作者：
Wormley Dd;S. Chirwa;T. Nayyar;J. Wu;S. Johnson;L. Brown;E. Harris;D. Hood
通讯作者：
Wormley Dd;S. Chirwa;T. Nayyar;J. Wu;S. Johnson;L. Brown;E. Harris;D. Hood

Downregulation of hippocampal NMDA receptor expression by prenatal exposure to dioxin.

产前接触二恶英导致海马 NMDA 受体表达下调。