L. Gail Darlington , Caroline M. Forrest , Gillian M. Mackay , Lynn Oxford , Nicholas Stoy , Trevor W. Stone
{"title":"骨质疏松症中犬尿氨酸途径代谢的解释","authors":"L. Gail Darlington , Caroline M. Forrest , Gillian M. Mackay , Lynn Oxford , Nicholas Stoy , 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":"{\"title\":\"Interpretation of kynurenine pathway metabolism in osteoporosis\",\"authors\":\"L. Gail Darlington , Caroline M. Forrest , Gillian M. Mackay , Lynn Oxford , Nicholas Stoy , 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}","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}
Interpretation of kynurenine pathway metabolism in osteoporosis
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.