Diminished quality of life in patients with cancer correlates with tryptophan degradation

Schroecksnadel, Katharina; Fiegl, Michael; Prassl, Karin; Winkler, Christiana; Denz, H.; Fuchs, Dietmar

doi:10.1007/s00432-007-0191-3

Cited by 48 publications

(56 citation statements)

References 34 publications

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“…In line with previous reports using plasma CRP levels and ESR to evaluate the association between the kynurenine pathway and inflammation, we found a strong relation between these inflammatory markers and parameters for TRP oxidation [27,28,36]. The correlation between the KYN/TRP ratio and the NLR, which is an index of systemic inflammatory response [37], additionally strengthens this association.…”

Section: Discussionsupporting

confidence: 88%

“…Relevant changes in TRP metabolism are known to occur in neurodegenerative disorders and psychiatric conditions, but also in malignancy, end-stage renal failure, inflammatory disease, epilepsy and trauma [2][3][4][5][6][7][8][9][10][27][28][29][30]. The involvement of the kynurenine pathway in acute ischemic stroke is under current investigation.…”

Section: Discussionmentioning

confidence: 99%

“…From October 2005 until February 2008, 156 patients were enrolled for analysis of KYN. Since the TRP metabolism may be influenced by the following conditions [2][3][4][5][6][7][8][9][10][27][28][29][30], patients with neurodegenerative disease (n = 3), major psychiatric disorders (n = 1), epilepsy (n = 1), premorbid inflammatory disease (n = 1), end-stage renal failure (n = 1), major trauma or sepsis (n = 0) were excluded from analysis. Stroke etiology was classified according to the TOAST criteria.…”

Section: Study Populationmentioning

confidence: 99%

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The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke

et al. 2010

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Post-stroke inflammation may induce upregulation of the kynurenine (KYN) pathway for tryptophan (TRP) oxidation, resulting in neuroprotective (kynurenic acid, KA) and neurotoxic metabolites (3-hydroxyanthranillic acid, 3-HAA). We investigated whether activity of the kynurenine pathway in acute ischemic stroke is related to initial stroke severity, long-term stroke outcome and the ischemia-induced inflammatory response. Plasma concentrations of TRP and its metabolites were measured in 149 stroke patients at admission, at 24 h, at 72 h and at day 7 after stroke onset. We evaluated the relation between the KYN/TRP ratio, the KA/3-HAA ratio and stroke severity, outcome and inflammatory parameters (C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and neutrophil/lymphocyte ratio (NLR)). KYN/TRP but not KA/3-HAA correlated with the NIHSS score and with the infarct volume. Patients with poor outcome had higher mean KYN/TRP ratios than patients with more favourable outcome. The KYN/TRP ratio at admission correlated with CRP levels, ESR and NLR. The activity of the kynurenine pathway for tryptophan degradation in acute ischemic stroke correlates with stroke severity and long-term stroke outcome. Tryptophan oxidation is related to the stroke-induced inflammatory response.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

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The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke

et al. 2010

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“…In cancer patients, higher concentrations of serum neopterin, which is produced in large amounts by human monocytes/macrophages upon stimulation by IFN-␥, were reported, and measurement of serum neopterin allows assessment of the endogenous production of IFN-␥ [11,12,19,21]. Fuchs et al reported a significant positive correlation between neopterin concentration and Kyn/Trp ratio in serum of patients with several cancers, suggesting that increased IFN-␥ production in cancer patients is responsible for higher IDO activity, in particular, in macrophages and DC [11,12,19,21]. However, in the present study no association was found between the serum concentrations of IFN-␥ and the IDO activity in patients with lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Increased serum kynurenine/tryptophan ratio correlates with disease progression in lung cancer

Suzuki¹,

Suda²,

Furuhashi³

et al. 2010

Lung Cancer

220

208

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“…Several studies have shown that modulated MPO levels and/or the acceleration of the rate of Trp degradation correlate with the extent of disease and predicting disease progression [3][4][5][6][7][8][9]. For example, cancer patients have enhanced degradation of Trp are not only found to predict shorter lifespan but are also associated with impaired quality of life [10][11][12]. In obesity, plasma tryptophan concentrations have been shown to be decreased and to be independent of weight reduction or dietary intake [13][14].…”

Section: Introductionmentioning

confidence: 99%

Potential role of tryptophan and chloride in the inhibition of human myeloperoxidase

Galijašević

Abdulhamid

Abu-Soûd

2008

Free Radical Biology and Medicine

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Myeloperoxidase (MPO) binds H 2 O 2 in the absence and presence of chloride (Cl − ) and catalyzes the formation of potent oxidants through 1e − and 2e − oxidation pathways. These potent oxidants have been implicated in the pathogenesis of various diseases including atherosclerosis, asthma, arthritis, and cancer. Thus, inhibition of MPO and its byproducts may have a much wide application in biological systems. Using direct rapid kinetic measurements and H 2 O 2 -selective electrodes, we showed that tryptophan (Trp), an essential amino acid, was linked kinetically to the inhibition of MPO catalysis under physiological-like conditions. Trp inactivated MPO in the absence and presence of plasma levels of chloride (Cl − ), in various degrees, through binding to MPO forming the inactive complexes, Trp-MPO and Trp-MPO-Cl, respectively; and accelerating MPO Compound II formation, an inactive form of MPO. Inactivation of MPO was mirrored by the direct conversion of MPO-Fe(III) to MPO Compound II without any sign of Compound I accumulation. This behavior indicates that Trp binding modulates the formation of MPO intermediates and their decay rates. Importantly, Trp is a poor substrate for MPO Compound II and has no role in destabilizing complex formation. Thus, the overall MPO catalytic activity will be limited by: 1) the dissociation of Trp from Trp-MPO and Trp-MPO-Cl complexes; 2) the affinity of MPO Compound I towards Cl − versus Trp; and 3) the slow conversion of MPO Compound II to MPO-Fe(III). Importantly, Trp dependentinhibition of MPO occurred with a wide range of concentrations that span various physiological and supplemental ranges.

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Diminished quality of life in patients with cancer correlates with tryptophan degradation

Abstract: Results suggest that immune-mediated tryptophan degradation may contribute to cancer-induced QoL deterioration.

Cited by 48 publications

References 34 publications

The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke

The Role of Tryptophan Catabolism along the Kynurenine Pathway in Acute Ischemic Stroke

Increased serum kynurenine/tryptophan ratio correlates with disease progression in lung cancer

Potential role of tryptophan and chloride in the inhibition of human myeloperoxidase

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