Tryptophan administration induces oxidative stress in brain cortex of rats

Feksa, Luciane Rosa; Latini, Alexandra; Rech, Virgínia Cielo; Feksa, Patrícia Bartels; Koch, Gustavo Duarte Waltereith; Amaral, Maria Fernanda Arévalo do; Leipnitz, Guilhian; Dutra-Filho, Carlos Severo; Wajner, Moaçir; Wannmacher, Clóvis Milton Duval

doi:10.1007/s11011-008-9087-4

Cited by 21 publications

(10 citation statements)

References 38 publications

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“…In addition, several studies have showed that tryptophan loading could induce oxidative stress in brain cortex of rats, and tryptophan metabolism may contribute to brain damage following stroke. [ 31 32 ] In the present study, we determined that several tryptophan metabolites were decreased during the early stage after ASCP that may alleviate brain oxidative damage. Besides, KYN has been known to play an important role in the process of neuronal damage and neurodegenerative disorders, and it could promote oxidative stress following a stroke.…”

Section: Discussionmentioning

confidence: 94%

Cerebral Metabolic Profiling of Hypothermic Circulatory Arrest with and Without Antegrade Selective Cerebral Perfusion

Zou

Liu

Zhang

et al. 2016

Chinese Medical Journal

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Background:Antegrade selective cerebral perfusion (ASCP) is regarded to perform cerebral protection during the thoracic aorta surgery as an adjunctive technique to deep hypothermic circulatory arrest (DHCA). However, brain metabolism profile after ASCP has not been systematically investigated by metabolomics technology.Methods:To clarify the metabolomics profiling of ASCP, 12 New Zealand white rabbits were randomly assigned into 60 min DHCA with (DHCA+ASCP [DA] group, n = 6) and without (DHCA [D] group, n = 6) ASCP according to the random number table. ASCP was conducted by cannulation on the right subclavian artery and cross-clamping of the innominate artery. Rabbits were sacrificed 60 min after weaning off cardiopulmonary bypass. The metabolic features of the cerebral cortex were analyzed by a nontargeted metabolic profiling strategy based on gas chromatography-mass spectrometry. Variable importance projection values exceeding 1.0 were selected as potentially changed metabolites, and then Student's t-test was applied to test for statistical significance between the two groups.Results:Metabolic profiling of brain was distinctive significantly between the two groups (Q2Y = 0.88 for partial least squares-DA model). In comparing to group D, 62 definable metabolites were varied significantly after ASCP, which were mainly related to amino acid metabolism, carbohydrate metabolism, and lipid metabolism. Kyoto Encyclopedia of Genes and Genomes analysis revealed that metabolic pathways after DHCA with ASCP were mainly involved in the activated glycolytic pathway, subdued anaerobic metabolism, and oxidative stress. In addition, L-kynurenine (P = 0.0019), 5-methoxyindole-3-acetic acid (P = 0.0499), and 5-hydroxyindole-3-acetic acid (P = 0.0495) in tryptophan metabolism pathways were decreased, and citrulline (P = 0.0158) in urea cycle was increased in group DA comparing to group D.Conclusions:The present study applied metabolomics analysis to identify the cerebral metabolic profiling in rabbits with ASCP, and the results may shed new lights that cerebral metabolism is better preserved by ASCP compared with DHCA alone.

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Section: Discussionmentioning

confidence: 94%

Cerebral Metabolic Profiling of Hypothermic Circulatory Arrest with and Without Antegrade Selective Cerebral Perfusion

Zou

Liu

Zhang

et al. 2016

Chinese Medical Journal

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“…TRP is widely available on the market as a supplement for both animals and humans. However, there have been concerns that excess administration of TRP may cause oxidative stress in the cerebral cortex (91), as well as other adverse effects, including ataxia, tremors, diaphoresis, blurred vision, dry mouth, muscle stiffness, palpitations, urticaria, and the "eosinophilia-myalgia syndrome" (EMS) (92)(93)(94)(95)(96)(97). However, some of these side effects might have been caused by contaminated substance(s) in the former TRP preparations, but not TRP itself.…”

Section: Safety Of Oral Trp and Its Metabolitesmentioning

confidence: 99%

Tryptophan metabolism in animals important roles in nutrition and health

Yao

Fang²,

Yin³

et al. 2011

Front Biosci

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L-Tryptophan is a nutritionally essential amino acid for monogastric animals and preweaning ruminants because it cannot be synthesized in the body. Besides serving as a building block for proteins, tryptophan is a critical nutrient for the functions of nervous and immune systems. Over the past decades, much attention has been directed to study the role of tryptophan as a limiting amino acid in mammalian and avian nutrition. However, emerging evidence from recent studies shows that tryptophan and its metabolites (e.g., serotonin (5-hydroxytryptamine, 5-HT) and melatonin)) can regulate feed intake, reproduction, immunity, neurological function, and anti-stress responses. Additionally, tryptophan may modulate gene expression and nutrient metabolism to impact whole-body homeostasis in organisms. Thus, adequate intake of this amino acid from the diet is crucial for growth, development, and health of animals and humans.

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“…Furthermore, oxidative stress due to Trp loading can also be prevented by the pretreatment with antioxidants. Thus the hypothesis of Trp-induced oxidative stress in brain cortex has been elucidated by giving taurine or alpha-tocopherol plus ascorbic acid (Feksa et al 2008 ). Nonspecifi c NOS inhibitors decrease the homocysteine-induced lipid peroxidation than does the selective neuronal NOS inhibitor.…”

Section: Hypertryptophanemiamentioning

confidence: 99%

Tryptophan and Cell Death

Engin¹

2015

Tryptophan Metabolism: Implications for Biological Processes, Health and Disease

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Cell death attributed to the tryptophan (Trp) metabolites is dependent on the exposure time and intracellular concentrations of cytotoxic Trp derivatives such as 3-hydroxykynurenine (3HK), 3-hydroxyanthranilic acid (3HAA), 5-hydroxyanthranilic acid (5HAA), and quinolinic acid (QA). However, 3HAA, 3HK, and QA at low concentrations may also serve as a precursor for nicotinamide adenine dinucleotide [NAD + ] which has vital importance to maintain cell viability. Inhibition of indoleamine 2,3-dioxygenase (IDO) activity results in a dosedependent decrease in intracellular [NAD + ] levels. Mitochondrial permeability transition occurs in several forms of necrotic cell death. Disturbances in the normal function of the mitochondria are associated with the alterations in the balance of Trp metabolism. While kynurenic acid (KA) has proven to be neuroprotective with the potential endogenous antioxidant properties, QA is a specifi c agonist at the N-methyl-d -aspartate (NMDA) receptors and a potent neurotoxin with the marked free radical-producing property. QA-induced cytotoxic effects are mediated by overactivation of NMDA-like receptors and overexpression of inducible nitric oxide synthase (iNOS). l -Kynurenine-derived neurotoxin-induced apoptosis occurs through reactive oxygen species (ROS)-mediated pathways and is blocked by antioxidants. Unlike the kynurenine pathway, the methoxyindole metabolites of Trp metabolism protect cells against oxidative stress-induced apoptosis. Furthermore, deprivation of Trp triggers autophagy in a mammalian target of rapamycin (mTOR)-dependent manner. mTOR inhibition can suppress the activation of cyclin-dependent kinases and then inhibits the cell cycle progress, suppresses cell proliferation, and fi nally results in cell apoptosis.

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Tryptophan administration induces oxidative stress in brain cortex of rats

Cited by 21 publications

References 38 publications

Cerebral Metabolic Profiling of Hypothermic Circulatory Arrest with and Without Antegrade Selective Cerebral Perfusion

Cerebral Metabolic Profiling of Hypothermic Circulatory Arrest with and Without Antegrade Selective Cerebral Perfusion

Tryptophan metabolism in animals important roles in nutrition and health

Tryptophan and Cell Death

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