Interpretation of kynurenine pathway metabolism in osteoporosis

L. Gail Darlington , Caroline M. Forrest , Gillian M. Mackay , Lynn Oxford , Nicholas Stoy , Trevor W. Stone
{"title":"Interpretation of kynurenine pathway metabolism in osteoporosis","authors":"L. Gail Darlington ,&nbsp;Caroline M. Forrest ,&nbsp;Gillian M. Mackay ,&nbsp;Lynn Oxford ,&nbsp;Nicholas Stoy ,&nbsp;Trevor W. Stone","doi":"10.1016/j.ics.2007.07.014","DOIUrl":null,"url":null,"abstract":"<div><p><span>Recent evidence that oxidative stress<span><span><span> may contribute to the development or progress of osteoporosis may indicate an underlying, or accompanying state of inflammation. In general, inflammatory conditions are associated with the activation of immune-competent cells in which activation of the </span>kynurenine<span> pathway occurs in parallel with the generation and release of cytokines and oxidative stress. We have therefore measured the levels of kynurenine pathway metabolites as well as peroxidation products and inflammatory markers such as </span></span>neopterin, </span></span>in patients<span><span> with osteoporosis before and after two years of drug treatment. At diagnosis, patients showed much higher levels of </span>anthranilic acid<span> than control subjects, but less 3-hydroxy-anthranilic acid. There were also high levels of lipid peroxidation products. All these parameters normalised over two years of treatment, together with a significant improvement in bone density assessed by dual energy X-ray absorptiometry (DEXA) scans. Here, we hypothesise that there may be a causal link between these factors.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 367-371"},"PeriodicalIF":0.0000,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.014","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International congress series","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0531513107004219","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

Abstract

Recent evidence that oxidative stress may contribute to the development or progress of osteoporosis may indicate an underlying, or accompanying state of inflammation. In general, inflammatory conditions are associated with the activation of immune-competent cells in which activation of the kynurenine pathway occurs in parallel with the generation and release of cytokines and oxidative stress. We have therefore measured the levels of kynurenine pathway metabolites as well as peroxidation products and inflammatory markers such as neopterin, in patients with osteoporosis before and after two years of drug treatment. At diagnosis, patients showed much higher levels of anthranilic acid than control subjects, but less 3-hydroxy-anthranilic acid. There were also high levels of lipid peroxidation products. All these parameters normalised over two years of treatment, together with a significant improvement in bone density assessed by dual energy X-ray absorptiometry (DEXA) scans. Here, we hypothesise that there may be a causal link between these factors.

骨质疏松症中犬尿氨酸途径代谢的解释
最近的证据表明,氧化应激可能有助于骨质疏松症的发展或进展,可能表明潜在的或伴随的炎症状态。一般来说,炎症与免疫能力细胞的激活有关,其中犬尿氨酸途径的激活与细胞因子和氧化应激的产生和释放同时发生。因此,我们测量了骨质疏松症患者在药物治疗前后两年的犬尿氨酸途径代谢物、过氧化产物和炎症标志物(如新蝶呤)的水平。诊断时,患者的邻氨基苯酸水平明显高于对照组,但3-羟基邻氨基苯酸水平较对照组低。脂质过氧化产物的含量也很高。经过两年的治疗,所有这些参数都正常化了,同时通过双能x线吸收仪(DEXA)扫描评估的骨密度也有了显著改善。在这里,我们假设这些因素之间可能存在因果关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信