Shigenobu Toné , Aurore Britan , Aicha Jrad , Violette Maffre , Joël R. Drevet
{"title":"The mouse epididymis: A site of strong and constitutive expression of the tryptophan metabolizing enzyme indoleamine 2,3-dioxygenase (IDO)","authors":"Shigenobu Toné , Aurore Britan , Aicha Jrad , Violette Maffre , Joël R. Drevet","doi":"10.1016/j.ics.2007.07.035","DOIUrl":"10.1016/j.ics.2007.07.035","url":null,"abstract":"<div><p>Some twenty-five years ago it was reported for the first time that indoleamine 2,3-dioxygenase (IDO) activity was particularly important in rodent epididymis<span><span> protein extracts. Several years ago, it was also shown that the epididymal expression of IDO was constitutive and not driven by the interferon-gamma, inflammatory cytokine, as is the case in most of the other tissues tested. Since then, the epididymal expression of IDO has not been investigated further. Recently, we have reported a more detailed study showing that indeed the mouse epididymis expresses both IDO transcript and protein at a high level while this is not the case for the other tryptophan-catabolizing </span>enzyme<span>, TDO. On the basis of the different functions that have been assigned to IDO we discuss here the putative roles of IDO expression as well as tryptophan metabolism on the physiology of the mammalian epididymis.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 233-240"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"100331366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Bertazzo , S. Comai , L. Cavalletto , L. Chemello , S. Luise , C.V.L. Costa
{"title":"Changes in serum tryptophan during antiviral therapy with recombinant α-interferon in chronic hepatitis C","authors":"A. Bertazzo , S. Comai , L. Cavalletto , L. Chemello , S. Luise , C.V.L. Costa","doi":"10.1016/j.ics.2007.07.008","DOIUrl":"10.1016/j.ics.2007.07.008","url":null,"abstract":"<div><p><span><span>The most effective treatment<span> of chronic hepatitis C (HCV) available to date is represented by interferon-α (IFN-α), alone or in combination with </span></span>ribavirin<span>. However, the therapy presents adverse effects<span><span>, including depressive symptoms. As IFN-α can cause an alteration of the tryptophan metabolism and a consequent reduced synthesis of serotonin, we have designed a study aimed to investigate the effect of IFN-α therapy on the serum levels of tryptophan and on the development of depression </span>in patients<span><span><span> affected by the hepatitis C virus. Nine patients with HCV were enrolled while treated with IFN-α2a (3 MU thrice/week) plus ribavirin (15 mg/kg/day) for six months. All patients were evaluated by a hepatologist and received two self-administered scales [Beck Depression Inventory (BDI) and </span>Hospital Anxiety and Depression Scale (HADS)]. Blood samples were collected before treatment and at one month and six months of therapy. Tryptophan, 5-hydroxytryptophan and serotonin were analysed by </span>HPLC with a spectrofluorometric detector. In all cases, a significant decrease of serum tryptophan concentrations from baseline (17.60</span></span></span></span> <!-->±<!--> <!-->1.08 mg/ml) to one month (13.94<!--> <!-->±<!--> <!-->1.18 mg/ml) and six months (12.68<!--> <!-->±<!--> <span>0.64 mg/ml) with an increase of symptoms of depression was obtained, whereas 5-hydroxytryptophan and serotonin levels did not show any variation during the therapy from baseline values. The preliminary results suggest that IFN-α plays a role in serum tryptophan reduction and the development of depressive symptoms.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 362-366"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"110626706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Down-regulation of the indoleamine 2,3-dioxygenase (IDO) transcription by tryptophan analogues","authors":"Takeaki Okamoto , Shigenobu Toné , Hiroaki Kanouchi , Fumio Ohyama , Yohsuke Minatogawa","doi":"10.1016/j.ics.2007.07.015","DOIUrl":"10.1016/j.ics.2007.07.015","url":null,"abstract":"<div><p><span><span><span><span>Indoleamine 2,3-dioxygenase (IDO; EC 1.13.11.42) is a rate-limiting enzyme involved in the catabolism of </span>tryptophan, which is an </span>essential amino acid<span>. It is induced under pathological conditions, such as the presence of viral infections or tumor cells. This enzyme is induced by IFN-γ in the mouse </span></span>rectal carcinoma cell line CMT-93. It is known that both 1-methyl-</span><span>l</span>-tryptophan (1-MT) and methylthiohydantoin-<span>dl</span><span>-tryptophan (MTH-trp) are tryptophan analogues, and are authentic inhibitors of the enzymatic activity of IDO. In this study, we examined the effects of both 1-MT and MTH-trp on the IFN-γ inducible IDO expression of CMT-93. As a result, the IFN-γ inducible IDO mRNA and the protein levels in CMT-93 were suppressed by 1-MT and MTH-trp, independently. Moreover, tryptophan (Trp), as a substrate of IDO, also suppressed IDO induction by IFN-γ at the transcriptional level. These results suggest that 1-MT and MTH-trp as inhibitors of IDO enzymatic activity, and Trp suppress IDO induction by IFN-γ at the transcriptional level.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 352-356"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"112897438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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 , Caroline M. Forrest , Gillian M. Mackay , Lynn Oxford , Nicholas Stoy , Trevor W. Stone","doi":"10.1016/j.ics.2007.07.014","DOIUrl":"10.1016/j.ics.2007.07.014","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":0.0,"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":null,"resultStr":null,"platform":"Semanticscholar","paperid":"95066668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Relationship between serum kynurenine concentration and exercise performance","authors":"Yasuhiro Itoh , Reiko Yonekura , Chiharu Kobayashi , Kuniaki Saito , Yoshito Oguri , Kaoru Kawai , Ryoji Teradaira , Yoichi Nagamura","doi":"10.1016/j.ics.2007.07.044","DOIUrl":"10.1016/j.ics.2007.07.044","url":null,"abstract":"<div><p><span>We have hypothesized that a close correlation exists between tryptophan metabolism, exercise performance and mood. Before and after a 20-km run, a POMS test and serum </span><span>l</span>-kynurenine determination were performed. Serum <span>l</span>-kynurenine concentration was negatively correlated with running distance. After running, scores for Vigor and serum <span>l</span>-kynurenine concentration were correlated (<em>r</em> <!-->=<!--> <!-->0.556); subjects with higher <span>l</span>-kynurenine concentrations tended to have higher scores for Vigor. In this study, we attempted to confirm this hypothesis. The present results suggest a close correlation between tryptophan metabolism, exercise performance and mood.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 167-170"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"100890693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Trichloroacetic acid-triggered reaction of kynurenine with nitrite produced by bone marrow-derived myeloid dendritic cells stimulated with CpG","authors":"Toshiaki Hara , Rie Hiramatsu , Hidetoshi Akimoto , Osamu Takikawa , Tsutomu Kawabe , Fumihiko Nagase","doi":"10.1016/j.ics.2007.07.027","DOIUrl":"10.1016/j.ics.2007.07.027","url":null,"abstract":"<div><p><span><span>Indoleamine 2,3-dioxygenase (IDO)-initiated tryptophan (Trp) metabolism along the </span>kynurenine<span><span> (Kyn) pathway regulates T cell responses. However, it is not clear whether bone marrow-derived </span>myeloid dendritic cells<span> (BMDC) express functional IDO. In this study, BMDC expressed IDO protein with nitric oxide (NO) production by </span></span></span>CpG oligodeoxynucleotides (CpG), and the CpG-mediated induction of IDO activity in BMDC was severely down-regulated by NO. The error in the estimation of Kyn assay was induced by the reaction of Kyn with nitrite under acidic conditions.</p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 205-208"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"95508540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chai K. Lim , George A. Smythe , Roland Stocker , Bruce J. Brew , Gilles J. Guillemin
{"title":"Characterization of the kynurenine pathway in human oligodendrocytes","authors":"Chai K. Lim , George A. Smythe , Roland Stocker , Bruce J. Brew , Gilles J. Guillemin","doi":"10.1016/j.ics.2007.07.011","DOIUrl":"10.1016/j.ics.2007.07.011","url":null,"abstract":"<div><p><span>It is important to understand the involvement of oligodendrocytes in the </span>kynurenine<span><span><span> pathway (KP) and more particularly, their potential ability to produce neuroprotective metabolites such as </span>kynurenic acid<span><span> (KYNA) or picolinic acid<span> (PIC), and the possibility of taking up and catabolizing the excitotoxin </span></span>quinolinic acid<span> (QUIN). These mechanisms may play a crucial role in the pathophysiology of neuroinflammatory diseases, especially </span></span></span>multiple sclerosis<span><span><span>. We used RT-PCR and HPLC to delineate KP </span>enzyme expression and KP metabolite production. We characterized the KP in oligodendrocytes and showed that they lack </span>IDO<span><span> expression and are unable to catabolize tryptophan. However, the other </span>enzymes in the pathway are present. These results indicate that human oligodendrocytes are more likely to produce neuroprotective KP metabolites such as KYNA and PIC rather than QUIN. However, because of the lack of IDO they are not able to down-regulate the immune response and as such may be more vulnerable to autoimmune phenomena.</span></span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 213-217"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"110472749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of melatonin on serum cholesterol status with formation of alpha-naphthylisothiocyanate-induced liver injury in rats","authors":"Yoshiji Ohta , Yoichiro Imai , Akira Kitagawa","doi":"10.1016/j.ics.2007.07.001","DOIUrl":"10.1016/j.ics.2007.07.001","url":null,"abstract":"<div><p><span>Liver injury with cholestasis<span> appeared 24 h, but not 12 h, after treatment of rats with alpha-naphthylisotiocyanate (ANIT) (75 mg/kg, i.p.). Serum total, free, and estrified cholesterol levels were unchanged at 12 h after ANIT treatment but increases in serum total and free cholesterol levels occurred at 24 h. </span></span>Melatonin<span> (100 mg/kg, p.o.) administered at 12 h after ANIT treatment significantly attenuated these increases at 24 h after the treatment. Thus, melatonin attenuates the disruption of serum cholesterol status with liver injury formation in rats treated with ANIT.</span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 380-383"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"110377228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Organ members (international/local)","authors":"","doi":"10.1016/S0531-5131(07)00471-2","DOIUrl":"https://doi.org/10.1016/S0531-5131(07)00471-2","url":null,"abstract":"","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages v-vii"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0531-5131(07)00471-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138342576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pharmacology of the kynurenine pathway","authors":"Trevor W. Stone , L. Gail Darlington","doi":"10.1016/j.ics.2007.07.013","DOIUrl":"10.1016/j.ics.2007.07.013","url":null,"abstract":"<div><p><span><span>The kynurenine<span><span> pathway of tryptophan </span>oxidative metabolism<span> plays a major role in the nervous and immune systems and has been implicated in a range of disease states. Much of the interest in the pathway has been centred around the role of quinolinic acid as an agonist at </span></span></span>glutamate receptors sensitive to </span><em>N</em>-methyl-<span>d</span><span>-aspartate (NMDA) and kynurenic acid<span><span> which blocks all the ionotropic glutamate receptors. In addition, it is clear that the pathway is important in modulating the level of oxidative stress in tissues, partly via the activation of blockade of NMDA receptors, but also via the generation of redox active compounds such as 3-hydroxykynurenine and 3-hydroxyanthranilic acid. Pharmacological interference with this pathway therefore presents a route for reducing oxidative tissue damage at several different metabolic steps, providing a valuable potential therapeutic target for new </span>drug development.</span></span></p></div>","PeriodicalId":84918,"journal":{"name":"International congress series","volume":"1304 ","pages":"Pages 298-304"},"PeriodicalIF":0.0,"publicationDate":"2007-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ics.2007.07.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"99816757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}