Day-to-day variation in urinary excretion of the histamine metabolite methylimidazoleacetic acid

1998 ◽  
Vol 47 (0) ◽  
pp. 52-53 ◽  
Author(s):  
G. Granerus ◽  
B. Lönnqvist
Keyword(s):  
Urinary Excretion ◽  
Histamine Metabolite ◽  
Methylimidazoleacetic Acid

The Urinary Excretion of 1-Methylimidazole-4-Acetic Acid, a Histamine Metabolite, by Healthy and Asthmatic Children

1973 ◽  
Vol 45 (2) ◽  
pp. 193-198
Author(s):  
Hazel Thom ◽  
Joyce E. Richardson ◽  
R. G. Mitchell
Keyword(s):  
Acetic Acid ◽  
Urinary Excretion ◽  
Statistical Difference ◽  
Control Group ◽  
Histamine Metabolism ◽  
Restricted Diet ◽  
Asthmatic Children ◽  
Histamine Metabolite ◽  
Methylation Pathway

1. The excretion of 1-methylimidazole-4-acetic acid (MeIAA) in urine was measured in three groups of asthmatic children (acute-symptoms, quiescent and steroid-treated) and a control group of hospitalized non-asthmatic children all on the same restricted diet. 2. There was no statistical difference between the excretion of MeIAA in urine in any of the groups. There was therefore no evidence of impairment of the methylation pathway of histamine metabolism in asthma.

Increased urinary excretion of the histamine metabolite Nι-methylhistamine during acetylsalicylic acid provocation in chronic urticaria patients

1990 ◽  
Vol 30 (1-2) ◽  
pp. 254-257 ◽  
Author(s):  
E. Oosting ◽  
S. H. Kardaun ◽  
H. M. G. Doeglas ◽  
P. Los ◽  
J. G. R. Monchy
Keyword(s):  
Urinary Excretion ◽  
Acetylsalicylic Acid ◽  
Chronic Urticaria ◽  
Histamine Metabolite

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

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