Effects of Tryptophan 2,3-Dioxygenase Inhibitors in the Rat

Salter, Mark; Beams, R. M.; Critchley, M. A. E.; Hodson, H. F.; Iyer, R.; Knowles, Richard G.; Madge, David J.; Pogson, Christopher I.

doi:10.1007/978-1-4684-5952-4_25

Cited by 4 publications

(2 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The first and rate-limiting step in this pathway is the conversion of Trp to N-formylkynurenine by indoleamine 2,3-dioxygenase (IDO) or tryptophan 2,3-dioxygenase (TDO) [80]. TDO exists primarily in liver [81] and can be activated by Trp [76] or corticosteroids [82], whereas IDO is found in numerous cell types, such as microglia, astrocytes, neurons [83] and macrophages [84] that reside in extra-hepatic tissues and is activated by pro-inflammatory signals [85, 86].…”

Section: Pathway and Enzymes To Make Nad+ From Tryptophanmentioning

confidence: 99%

NAD + metabolism: Bioenergetics, signaling and manipulation for therapy

Yang

Sauve

2016

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

385

307

View full text Add to dashboard Cite

We survey the historical development of scientific knowledge surrounding Vitamin B3, and describe the active metabolite forms of Vitamin B3, the pyridine dinucleotides NAD+ and NADP+ which are essential to cellular processes of energy metabolism, cell protection and biosynthesis. The study of NAD+ has become reinvigorated by new understandings that dynamics within NAD+ metabolism trigger major signaling processes coupled to effectors (sirtuins, PARPs, and CD38) that reprogram cellular metabolism using NAD+ as an effector substrate. Cellular adaptations include stimulation of mitochondrial biogenesis, a process fundamental to adjusting cellular and tissue physiology to reduced nutrient availability and/or increased energy demand. Several metabolic pathways converge to NAD+, including tryptophan-derived de novo pathways, nicotinamide salvage pathways, nicotinic acid salvage and nucleoside salvage pathways incorporating nicotinamide riboside and nicotinic acid riboside. Key discoveries highlight a therapeutic potential for targeting NAD+ biosynthetic pathways for treatment of human diseases. A recent emergence of understanding that NAD+ homeostasis is vulnerable to aging and disease processes has stimulated testing to determine if replenishment or augmentation of cellular or tissue NAD+ can have ameliorative effects on aging or disease phenotypes. This experimental approach has provided several proof of concept successes demonstrating that replenishment or augmentation of NAD+ concentrations can provide ameliorative or curative benefits. Thus NAD+ metabolic pathways can provide key biomarkers and parameters for assessing and modulating organism health.

show abstract

Section: Pathway and Enzymes To Make Nad+ From Tryptophanmentioning

confidence: 99%

NAD + metabolism: Bioenergetics, signaling and manipulation for therapy

Yang

Sauve

2016

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

385

307

View full text Add to dashboard Cite

show abstract

“…The eight-step de novo synthesis pathway is initiated by indoleamine 2,3-dioxygenase (IDO) or tryptophan 2,3-dioxygenase (TDO) that convert tryptophan to N-formylkynurenine (Salter et al, 1991). Through formamidase (KFase), N-formylkynurenine is then transformed to be kynurenine, to which hydroxyl is added via kynurenine 3hydroxylase (K3H).…”

Section: De Novo Synthesis From Tryptophanmentioning

confidence: 99%

Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

Hong

Zhang

et al. 2020

Front. Cell Dev. Biol.

124

View full text Add to dashboard Cite

NAD+, a co-enzyme involved in a great deal of biochemical reactions, has been found to be a network node of diverse biological processes. In mammalian cells, NAD+ is synthetized, predominantly through NMN, to replenish the consumption by NADase participating in physiologic processes including DNA repair, metabolism, and cell death. Correspondingly, aberrant NAD+ metabolism is observed in many diseases. In this review, we discuss how the homeostasis of NAD+ is maintained in healthy condition and provide several age-related pathological examples related with NAD+ unbalance. The sirtuins family, whose functions are NAD-dependent, is also reviewed. Administration of NMN surprisingly demonstrated amelioration of the pathological conditions in some agerelated disease mouse models. Further clinical trials have been launched to investigate the safety and benefits of NMN. The NAD+ production and consumption pathways including NMN are essential for more precise understanding and therapy of age-related pathological processes such as diabetes, ischemia-reperfusion injury, heart failure, Alzheimer's disease, and retinal degeneration.

show abstract

Metabolism and Biology of Tryptophan

Brown

1996

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

Effects of Tryptophan 2,3-Dioxygenase Inhibitors in the Rat

Cited by 4 publications

References 14 publications

NAD + metabolism: Bioenergetics, signaling and manipulation for therapy

NAD + metabolism: Bioenergetics, signaling and manipulation for therapy

Nicotinamide Mononucleotide: A Promising Molecule for Therapy of Diverse Diseases by Targeting NAD+ Metabolism

Metabolism and Biology of Tryptophan

Contact Info

Product

Resources

About