The regulation of tryptophan pyrrolase activity by tryptophan
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Cited by (68)
Kynurenine pathway and human systems
2020, Experimental GerontologyCitation Excerpt :Thus, loss of this induction mechanism underpins Trp toxicity. For example, adrenalectomy renders the rat vulnerable to Trp toxicity and cortisol administration to adrenalectomized rats restores safety (Knox, 1966). This protective effect of TDO does not apply to IDO for 2 reasons: (1) Trp-sensitive species are vulnerable to Trp toxicity despite having a higher IDO activity than rats; (2) as stated above, [Trp] ≥ 50 μM inhibits IDO activity.
Hypothesis: Metabolic targeting of 5-aminolevulinate synthase by tryptophan and inhibitors of heme utilisation by tryptophan 2,3-dioxygenase as potential therapies of acute hepatic porphyrias
2019, Medical HypothesesCitation Excerpt :Glucocorticoids: Glucocorticoids that induce TDO synthesis and hence utilisation of the regulatory-heme pool should be considered unsafe or usable with caution in acute hepatic porphyrias. TDO induction has been demonstrated with the natural glucocorticoids corticosterone [70], cortisone [120] and cortisol [121] and the synthetic ones prednisolone [122], dexamethasone [123] and triamcinolone [124]. The permissive effect of glucocorticoids on 5-ALAS induction by the porphyrogen AIA has been documented.
The good and bad of antioxidant foods: An immunological perspective
2015, Food and Chemical ToxicologyCitation Excerpt :This is necessary, as also tryptophan 2,3-dioxygenase (TDO) can degrade tryptophan. TDO is expressed in the liver and is regulated by tryptophan levels and glucocorticoids (Knox, 1966). During immune response, IFN-γ released by T cells induces high output of ROS by human macrophages.
Purification and kinetic characterization of human indoleamine 2,3-dioxygenases 1 and 2 (IDO1 and IDO2) and discovery of selective IDO1 inhibitors
2011, Biochimica et Biophysica Acta - Proteins and ProteomicsHepatic alteration of tryptophan metabolism in an acute porphyria model. Its relation with gluconeogenic blockage
2008, Biochemical PharmacologyCitation Excerpt :This moderate TRP accumulation would trigger TRPp enhancement. In fact, it has been reported that TRP produces a substrate-type TRPp enhancement involving the reduced degradation of the preexisting apoenzyme at a normal synthesis rate [20,21,23]. The effects caused by moderate increases of TRP hepatic concentration in vivo such as those observed in the porphyria model studied, together with the activation of the enzyme in vitro, have been suggested to be involved in the promotion of the apoenzyme conjugation with heme and the subsequent reduction of the oxidized holoenzyme [23].