Plasma tryptophan and anorexia in human cancer

Fanelli, Filippo Rossi; Cangiano, C.; Ceci, Fabrizio; Cellerino, R; Franchi, F; Menichetti, E; Muscaritoli, Maurizio; Cascino, A.

doi:10.1016/0277-5379(86)90346-9

Cited by 67 publications

(24 citation statements)

References 25 publications

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“…We cannot explain the difference between our results and some earlier reported findings of elevated levels of plasma free tryptophan in animals (Krause et al, 1979) and patients (Cangiano et al, 1990) with cancer -particularly those with anorexia (Chance et al, 1983;Fanelli et al, 1986). In the present study, laboratory analysis was carried out on mixed batches of control and cancer patient samples without knowledge of the patient source.…”

Section: Discussioncontrasting

confidence: 61%

Serum tryptophan decrease correlates with immune activation and impaired quality of life in colorectal cancer

et al. 2002

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Cancer-related indoleamine (2,3)-dioxygenase up-regulation by interferon-g might influence quality of life by depleting serum tryptophan. We correlated serum tryptophan levels with immune activation and quality of life in patients with colorectal liver metastases. Venous blood was sampled from patients with primary colorectal cancer and from patients with metachronous colorectal liver metastases who completed quality of life and psychological questionnaires. Serum tryptophan, kynurenine, neopterin, interleukin 2 soluble receptor a (IL-2 sRa), soluble tumour necrosis factor receptor I (sTNF RI), interleukin 6, and C-reactive protein were measured. Liver metastasis volume was estimated by computerised tomography, and survival from blood sampling was noted. Sixty-six patients with colorectal cancer were studied (39 males; median age 66 years) of whom 25 had colorectal liver metastases only (17 males; median age 62 years; median liver metastasis volume 208 ml; median survival 234 days). Reduced serum tryptophan was significantly associated with Rotterdam Symptom Checklist physical symptom (r=70.51, P=0.01) and Sickness Impact Profile (r=70.42, P=0.04) scores, and correlated with increased serum neopterin (r=70.36, P=0.003), IL-2 sRa (r=70.51, P=0.01) and sTNF RI (r=70.45, P=0.02) levels. Stepwise regression analyses suggested that serum tryptophan was an independent predictor of Rotterdam Symptom Checklist physical symptom (regression coefficient 720.78, P=0.01) and Sickness Impact Profile (regression coefficient 7109.09, P=0.04) scores. The results supported a role for interferon-g-mediated serum tryptophan decrease in cancer-induced quality of life deterioration.

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Section: Discussioncontrasting

confidence: 61%

Serum tryptophan decrease correlates with immune activation and impaired quality of life in colorectal cancer

et al. 2002

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“…Krause et al [1979] reported a correlation between anorexia and brain levels of tryptophan and serotonin in tumor-bearing animals and proposed that an increase in brain serotonin synthesis may be, in part, responsible for the onset of cancer anorexia [Krause et al, 1981]. This hypothesis may also hold true in humans [Fanelli et al, 1986], because plasma levels of free tryptophan were significantly increased in anorectic cancer patients and seemed to confirm that free tryptophan may play a role in cancer anorexia in humans.…”

Section: Other Physiological Actions Of Tryptophan Metabolitesmentioning

confidence: 65%

Possible roles of excess tryptophan metabolites in cancer

Chung

Gadupudi

2011

Environ and Mol Mutagen

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Tryptophan is metabolized through serotonin, indole, and kynurenine (KN) pathways. Uptake of an excess amount of tryptophan accompanied with vitamin B6 deficiency may result in the accumulation of higher concentrations of metabolites mainly from the KN pathways in the bladder. These metabolites could interact with nitrite to become mutagenic nitrosamines. They could be a promoter in the initiator-promoter model of carcinogenesis. They produced bladder cancer when implanted in the bladder. They also interact with transition metals copper or iron to form reactive radicals or reactive oxygen species (ROS). Some metabolites, 3-hydroxy-anthranilic acid, were autooxidized to mutagenic cinnabarinic and anthranilyl radical intermediates. These radical intermediates could also be ligands that interact with aryl hydrocarbon receptor (AhR) and induce xenobiotic metabolizing enzymes (XMEs) to metabolize contaminated carcinogens. When tryptophan is exposed to either visible or UV light, a photoproduct of 6-formylindolo[3,2b]-carbazole is formed, which has a very high affinity for the AhR that plays a role in carcinogenesis. This review gives an insight into various mechanisms through which tryptophan metabolites cause carcinogenesis. It could be concluded that tryptophan metabolites play a complementary role in promoting carcinogenesis along with carcinogens like aflatoxin, CCl(4) , 2-acetylaminofluorene, 4-aminobiphenyl, 2-naphthylamine, or N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide. The underlying mechanisms could be their autoxidation, exposure to either visible or UV light, interaction with nitrite or transition metals to form reactive intermediates, serving as ligands to interact with an AhR that is known to play a role in carcinogenesis through induction of XMEs. Further research is warranted.Environ.

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“…The presence of anorexia can be characterized by identification of objective symptoms, including early satiety, taste and smell alterations, meat aversion and nausea/vomiting. 9 The presence of anorexia is an extremely distressing syndrome, because appetite and the ability to eat have been reported to be the most important factors in the physical and psychological aspects of a patient's quality of life. 10 In anorexic cancer patients, early satiety together with a reduced appetite has been postulated to be caused by the production of factors by the tumor that exert their effects by acting on the hypothalamic sensory cells.…”

Section: Introductionmentioning

confidence: 99%