Urinary excretion of histamine, methylhistamine (1-MeHi) and methylimidazoleacetic acid (MeImAA) in mastocytosis: Comparison of new HPLC methods with other present methods

1984 ◽  
Vol 14 (3-4) ◽  
pp. 341-345 ◽  
Author(s):  
Göran Granerus ◽  
Urban Wass
Keyword(s):  
Urinary Excretion ◽  
Methylimidazoleacetic Acid

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.

Cigarette Smoking Increases Thromboxane A2 Formation without Affecting Platelet Survival in Young Healthy Females

1992 ◽  
Vol 68 (05) ◽  
pp. 583-588 ◽  
Author(s):  
Annika Dotevall ◽  
Christina Rångemark ◽  
Elsa Eriksson ◽  
Jack Kutti ◽  
Hans Wadenvik ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cigarette Smoking ◽  
Blood Cell ◽  
Urinary Excretion ◽  
Life Span ◽  
Cell Count ◽  
Thromboxane A2 ◽  
Blood Cell Count ◽  
Platelet Activity ◽  
Pai 1

SummarySmoking is a risk factor for the development of atherosclerotic cardiovascular disease, in men as well as in women. An increased urinary excretion of the thromboxane metabolite 2,3-dinor-thromboxane B2 (Tx-M) has been observed in smokers of both genders, suggesting that cigarette smoking may facilitate cardiovascular disease via an action on the platelets. The present study addressed the hypothesis that the increased Tx-M excretion in female smokers reflects a true facilitation of platelet reactivity in vivo, rather than an increased destruction of the platelets. In healthy female volunteers (aged 20–46 years, 18 smokers and 17 non-smokers) platelet life-span and indices of platelet activity were determined, together with plasma levels of plasminogen activator inhibitor-1 (PAI-1), fibrinogen, peripheral blood cell counts and hematocrit. The urinary excretion of Tx-M was higher in smokers than in non-smokers (361 vs. 204 pg/mg creatinine, respectively, p <0.05), while plasma and urinary β-thromboglobulin, plasma platelet factor 4, platelet mean life-span and platelet production rate did not differ between the groups. PAI-1 activity, white blood cell count and hematocrit were higher in smokers than in non-smokers (p <0.05). These data indicate that smoking facilitates platelet formation of thromboxane A2 without affecting platelet survival; i.e. it increases the activity of platelets without affecting their viability to a measurable extent. Such an increase in platelet activity, operating in parallel to a reduced fibrinolytic activity and a higher hematocrit and white blood cell count, may play an etiological role in smoking-induced cardiovascular disease in women.

ON THE VALUE OF SOME PARAMETERS OF ADRENOCORTICAL GLUCOCORTICOID FUNCTION

1963 ◽  
Vol 44 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. Van Der Straeten ◽  
A. Vermeulen ◽  
N. Orie ◽  
P. Regniers
Keyword(s):  
Urinary Excretion ◽  
Adrenal Cortex ◽  
Isotope Dilution ◽  
Isotope Dilution Method ◽  
Dilution Method ◽  
Steroid Excretion ◽  
Colorimetric Methods

ABSTRACT The authors studied the correlation between cortisol production, as measured by an isotope dilution method, and the urinary excretion of total and free Porter-Silber chromogens, as well as of 17-ketogenic steroids. Although a significant correlation exists between total Porter-Silber chromogens, 17-ketogenic steroid excretion and cortisol production, discrepancies are occasionally observed. Hence, different colorimetric methods should be used to assess the glucocorticoid activity of the adrenal cortex.

METABOLIC STUDIES WITH METHANDROSTENOLONE (17β-HYDROXY-17α-METHYL-ANDROSTA-1,4-DIEN-3-ONE) IN HUMAN SUBJECTS

1961 ◽  
Vol 38 (3) ◽  
pp. 413-418 ◽  
Author(s):  
S. Almqvist ◽  
D. Ikkos ◽  
R. Luft
Keyword(s):  
Urinary Excretion ◽  
Testosterone Propionate ◽  
Human Subjects ◽  
Calcium Retention ◽  
Metabolic Studies ◽  
Daily Dose

ABSTRACT The effect of graded doses (5, 10 and 25 mg/d of methandrostenolone and of 25 mg/d of testosterone propionate were compared in each of three metabolically stable adult subjects. Five mg/d of methandrostenolone induced nitrogen and calcium retention. The effects observed with larger doses of methandrostenolone (10 and 25 mg/d) were not quantitatively different from those with 5 mg/d. The nitrogen and calcium retention obtained with the daily dose of 5 mg of methandrostenolone was as great or greater than that induced by testosterone propionate (25 mg/d). Methandrostenolone induced creatinuria but had no effect on sodium and chloride balances and urinary excretion of 17-ketosteroids.

SOME EFFECTS OF PERCHLORATE ON THE DISTRIBUTION OF 131-IODIDE

1965 ◽  
Vol 50 (2) ◽  
pp. 195-201 ◽  
Author(s):  
E. Schönbaum ◽  
E. A. Sellers ◽  
M.J. Gill
Keyword(s):  
Urinary Excretion ◽  
Renal Excretion ◽  
Kidney Tissue ◽  
Intraperitoneal Dose ◽  
Blood Radioactivity ◽  
Radioactivity Levels

ABSTRACT The distribution of an intraperitoneal dose of 131-iodide was studied in rats receiving perchlorate. The accumulation of radioactivity in the stomach, which occurred soon after injection in controls, was inhibited by perchlorate. Concurrent with this, radioactivity in blood was higher in perchlorate treated rats than in controls. After perchlorate, more radioactivity in kidney tissue and an elevated urinary excretion of the tracer was noted. After 24 hours, plasma radioactivity was lower in perchlorate treated rats than in controls. Increased renal excretion of 131I after perchlorate is, at least in part, due to higher blood radioactivity levels, probably because of decreased iodide space due to the action of perchlorate.

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