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Natural Plant Dyes of Oriental Carpets
Published in Raymond Cooper, Jeffrey John Deakin, Natural Products of Silk Road Plants, 2020
The precursor of indigo is called indican, which is a colorless organic compound and soluble in water. Indican is a glycoside and thus, undergoes hydrolysis to yield glucose and a molecule known as indoxyl in which the chromophore is located. Upon exposure to air, indoxyl is readily oxidized to indigo.
Methods for the Analysis of Gastrointestinal Function
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Urinalyses may also be performed to detect an excessive growth of bacteria in the small intestines [51]. Analysis for the presence of indican (indoxyl sulfate) may be conducted. Indoles are produced by bacteria, particularly Escherichia coli and Bacterroides.
Kidney Function and Uremia
Published in Sirshendu De, Anirban Roy, Hemodialysis Membranes, 2017
This belongs to the group known as indoles. Indoxyl sulfate, tryptophan, melatonin, and indole-3-acetic acid are all indoles. Indoxyl sulfate enhances drug toxicity, inhibiting active tubular secretion and deiodination.8,9 It is also suspected to be one of the agents behind glomerular sclerosis,10 affecting the function of cellular organic acid. Due to protein binding, the percentage clearance of indoxyl sulfate is greatly reduced and can be as low as 0%–20%.
Hepcidin as a therapeutic target for anemia and inflammation associated with chronic kidney disease
Published in Expert Opinion on Therapeutic Targets, 2019
Jolanta Malyszko, Jacek S. Malyszko, Joanna Matuszkiewicz-Rowinska
They found that indoxyl sulfate increased hepcidin expression in a dose-dependent manner. Furthermore, silencing of the aryl hydrocarbon receptor (AhR) inhibited indoxyl sulfate-induced hepcidin expression. Moreover, Hamano et al. [64] demonstrated that absorbents of indoxyl sulfate, anti-inflammatory measures or AhR inhibitors, could be therapeutic. In animal model. AST-120 an oral adsorbent of the uremic toxin, reduced elevated hepcidin levels in adenine-induced CKD mice. Finally, they concluded that indoxyl sulfate affects iron metabolism in CKD by participating in hepcidin regulation via pathways that depend on AhR and oxidative stress. They also reported in in vitro experiments using EPO-producing HepG2 cells [65]. Moreover, iron treatment augmented oxidative stress, and iron-induced reduction of EPO and HIF-2α expression was restored by tempol, an antioxidant compound.
Microbiota-derived uremic retention solutes: perpetrators of altered nonrenal drug clearance in kidney disease
Published in Expert Review of Clinical Pharmacology, 2018
Alexander J Prokopienko, Thomas D Nolin
Microbiota-derived uremic toxins also affect CYP1A activity and expression [47,55,58,60,61], with idole-3-acetic acid and indoxyl sulfate being the most potent. Indole-3-acetic acid decreases CYP1A2 activity by 50% in human microsomes [61]. A combination of hippuric acid, indoxyl sulfate, and p-cresol also inhibit CYP1A2 activity in human microsomes [47]. However, contradictory findings have been reported, as indole-3-acetic acid and indoxyl sulfate individually have been shown to increase mRNA expression and enzyme activity of CYP1A2 [55,60]. Although reasons for the disparate findings are unclear, it likely involves the AhR nuclear receptor – a master regulator that activates CYP1A gene expression. Indoxyl sulfate is both a potent activating ligand of AhR that leads to increased expression of CYP1A2, and a direct inhibitor of CYP1A2 activity [55,60]. Because of this, investigators should consider incubations that are long enough in duration to induce expression when assessing the effect of indoxyl sulfate on CYP1A2. The sum of data suggest that microbiota-derived toxins inhibit CYP1A2 enzymatic activity and that indoxyl sulfate induces CYP1A2 functional expression.
The role of microbiota in allogeneic hematopoietic stem cell transplantation
Published in Expert Opinion on Biological Therapy, 2021
Chia-Chi Chang, Eiko Hayase, Robert R. Jenq
Indole is a metabolite produced by bacteria during degradation of tryptophan. Intestinal bacteria that express tryptophanase can catabolize tryptophan to produce indole and indole derivatives [63], which include indole-3-carboxaldehyde (ICA), was shown to reduce damage to IECs damage and reduced subsequent GVHD in mice after allo-HSCT [64]. Indole is metabolized by the liver into 3-indoxyl sulfate (3-IS), and is ultimately excreted in the urine in humans [10]. In a recent study, lower 3-IS levels detected in the urine within the first 10 days after allo-HSCT were associated with significantly higher transplant-related mortality and poor overall survival due to an increase in intestinal GVHD [10]. Interestingly, this study found that a higher abundances of Lachnospiraceae and Ruminococcaceae, which are members of the order of Clostridiales, was associated with higher urinary 3-IS levels; thus, lower urinary levels of 3-IS indicate that there may be reductions in Clostridiales within the microbiome [10]. Michonneau et al [9] reported that additional tryptophan-derived metabolites (indoleacetate, indoleacetylglutamine, and indolepropionate) were depleted in patients with active acute GVHD. Notably, these compounds are known to act as ligands for the aryl hydrocarbon receptor (AhR) and can regulate allogeneic T cell reactivity, and thus low levels seen during acute GVHD could contribute to GVHD physiology [9]. Together, these studies demonstrate that a variety of microbial-derived metabolites are capable of modulating acute GVHD severity in mouse models and may be potential targets for preventing or treating acute GVHD in patients.