Kynurenine Pathway Enzymes in Guinea pigs

Allegri, Graziella; Costa, Carlo Virgilio Luigi; Ragazzi, Eugenio; Bertazzo, Antonella; Biasiolo, M.

doi:10.1007/978-1-4615-0135-0_54

Cited by 3 publications

(2 citation statements)

References 18 publications

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“…Unfortunately, we have now observed that only modest changes in blood and bone marrow NAD + levels result from niacin deficiency in the guinea-pig, with a variable time course of depletion and a strong dependence on the tryptophan content of the diet. Coinciding with our completion of the animal-feeding part of this research, Allegri et al (2003) published a manuscript showing that guinea-pigs express a suitable range of enzymes in the kynurenine pathway to allow tryptophan to niacin conversion, which is in agreement with our findings.…”

Section: Discussionsupporting

confidence: 85%

The guinea-pig is a poor animal model for studies of niacin deficiency and presents challenges in any study using purified diets

2007

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The guinea-pig was previously reported as being sensitive to a niacin-deficient (ND), high-protein diet, suggesting that it is a suitable model for the low tryptophan to NAD þ conversion observed in human subjects. However, these studies were based on growth rates and mortality. The objective of the present study was to determine whether guinea-pigs are suitable for ND studies based on measurements of blood and bone marrow NAD þ . Using a 20 % casein diet, ND decreased blood NAD þ after 4 weeks, but this parameter returned to normal after 9 weeks of feeding, while bone marrow was decreased by 35 % at this time point. Using a 15 % casein diet, 7 weeks of ND caused 44 and 42 % decreases in blood and bone marrow NAD þ . Using a 10 % casein diet, ND decreased NAD þ by 32 % in blood and 62 % in bone marrow at 7 weeks. Growth rates were directly related to the dietary tryptophan content, with the lowest growth rates seen with the 10 % casein diet. Changes in guinea-pig NAD þ are comparable with the rat model at similar levels of dietary tryptophan, while mortality rates were dramatically higher in the guinea-pig model. The present study concludes that mortality in ND guinea-pigs is not indicative of poor tryptophan conversion, but is due to environmental stresses in guinea-pigs that are not observed with rats. We conclude that guinea-pigs are not suitable for research on niacin deficiency and they present challenges for any study requiring purified diets and wire-bottomed cages.

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Section: Discussionsupporting

confidence: 85%

The guinea-pig is a poor animal model for studies of niacin deficiency and presents challenges in any study using purified diets

2007

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“…Human astrocytes are unable to produce QUIN. However, non‐human astrocytes may be able to do so given the known inter‐species variation in KP enzyme expression [49,50,52,53,59–62]. There are conflicting results from several studies in mouse, rat, gerbil and human astrocytes and also between human primary astrocytes and astroglioma cell lines.…”

Section: What Is Known and What Is New About Quinolinic Acid Biosynthmentioning

confidence: 99%

Quinolinic acid, the inescapable neurotoxin

2012

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Over the last two decades, evidence for the involvement of quinolinic acid (QUIN) in neuroinflammatory diseases has been exponentially increasing. Within the brain, QUIN is produced and released by infiltrating macrophages and activated microglia, the very cells that are prominent during neuroinflammation. QUIN acts as an agonist of the N-methyl-D-aspartate receptor and as such is considered to be a brain endogenous excitotoxin. Since the discovery of the excitotoxic activity of QUIN in the early 1980s, several other cytotoxic mechanisms have been identified. We know today that QUIN acts as a neurotoxin, gliotoxin, proinflammatory mediator, prooxidant molecule and can alter the integrity and cohesion of the bloodbrain barrier. This paper aims to review some of the most recent findings about the effects of QUIN and its mode of action.

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Involvement of quinolinic acid in aids dementia complex

2005

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Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous brain excitotoxin when produced and released by activated macrophages/microglia, the very cells that are prominent in the pathogenesis of ADC. This review examines QUIN's involvement in the features of ADC and its role in pathogenesis. We then synthesize these findings into a hypothetical model for the role played by QUIN in ADC, and discuss the implications of this model for ADC and other inflammatory brain diseases.

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Kynurenine Pathway Enzymes in Guinea pigs

Cited by 3 publications

References 18 publications

The guinea-pig is a poor animal model for studies of niacin deficiency and presents challenges in any study using purified diets

The guinea-pig is a poor animal model for studies of niacin deficiency and presents challenges in any study using purified diets

Quinolinic acid, the inescapable neurotoxin

Involvement of quinolinic acid in aids dementia complex

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