Enzymes That Control the Conversion ofL-Tryptophan-nicotinamide and the Urinary Excretion Ratio (N1-Methyl-2-pyridone-5-carboxamide +N1-Methyl-4-pyridone-3-carboxamide)/N1-Methylnicotinamide in Mice

2013 ◽  
Vol 77 (10) ◽  
pp. 2105-2111 ◽  
Author(s):  
Katsumi SHIBATA ◽  
Nobuya MORITA ◽  
Yoshika SHIBATA ◽  
Tsutomu FUKUWATARI
Keyword(s):  
Urinary Excretion ◽  
Excretion Ratio

Measurements of Myofibrillar Protein Breakdown in Newborn Human Infants

1982 ◽  
Vol 63 (5) ◽  
pp. 421-427 ◽  
Author(s):  
J. L. Burgoyne ◽  
F. J. Ballard ◽  
F. M. Tomas ◽  
A. Dobozy ◽  
A. H. MacLennan ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Degradation Rate ◽  
Myofibrillar Protein ◽  
Full Term ◽  
Protein Breakdown ◽  
Excretion Ratio ◽  
Human Infants ◽  
Term Infants ◽  
Breakdown Rate ◽  
Ion Exchange Separation

1. Myofibrillar protein breakdown was calculated from the urinary excretion ratio of Nτ-methylhistidine (3-methylhistidine) to creatinine in newborn premature and full-term infants. Representative values were obtained from single voidings provided that the infant's metabolic status was stable. 2. Nτ-Methylhistidine in infant urine was measured by a rapid Auto Analyser method and shown to give similar values to those obtained by ion-exchange separation techniques. 3. The molar excretion ratio of Nτ-methylhistidine to creatinine averaged 0·0159 in urine samples obtained within 12 h after birth. A similar ratio was found in amniotic fluid collected at birth. It is argued that this ratio does not reflect a low rate of myofibrillar protein breakdown in the foetus, but rather a more effective transplacental passage of Nτ-methylhistidine than of creatinine. 4. The urinary ratio increased during the first 2 days after birth to a plateau at 0·0372. This represents a myofibrillar protein degradation rate of 3·40% day−1 in full-term infants. 5. The molar excretion ratio during the period 40–120 h after birth increased in premature infants and reflects a fractional degradation rate of 5·34% day−1 in those infants weighing less than 1 kg at birth. 6. Lower excretion ratios were found in some infants of diabetic mothers and in athyroid infants. 7. The urinary excretion ratio of Nτ-methylhistidine to creatinine is presented as a useful method for evaluating the breakdown rate of myofibrillar protein in neonates and can be applied to a number of abnormal nutritional or hormonal states.

Intestinal Permeability in Runners in the 1996 Chicago Marathon

1999 ◽  
Vol 9 (4) ◽  
pp. 426-433 ◽  
Author(s):  
Rachel D. Smetanka ◽  
C. Patrick Lambert ◽  
Robert Murray ◽  
Dennis Eddy ◽  
Mary Horn ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Intestinal Permeability ◽  
Prolonged Exercise ◽  
Test Solution ◽  
Distance Runners ◽  
Excretion Ratio ◽  
Long Distance ◽  
Gi Symptoms ◽  
Aspirin Ingestion ◽  
Gastrointestinal Permeability

Abdominal cramping, nausea, diarrhea, and GI bleeding are often reported in long-distance runners. This study set out to determine the effects of prolonged (2-4 hrs) exercise and NSAID ingestion on gastric and intestinal permeability during the first 5 hrs following the 1996 Chicago Marathon. Thirty-four healthy volunteers (20 M, 14 F; ages 30-50) completed the race and ingested the test solution (5 g sucrose, 5 g lactulose, 2 g rhamnose, in 40 ml water) within 10-15 min. The urinary excretion ratio of lactulose/rhamnose was used to assess small intestine permeability; sucrose excretion was used to evaluate gastric impairment. There were no significant differences for mean training mileage, postrace rectal temperature, and percent dehydration between runners who ingested NSAIDs and those who did not. In all, 75% of subjects reported aspirin or ibuprofen ingestion before or during the race. Runners who ingested ibuprofen had significant elevations in urinary lactulose excretion and lactulose/rhamnose ratio, whereas those who ingested aspirin or who did not ingest either NSAID had no significant differences in urinary excretion of lactulose, rhamnose, sucrose, or lactulose/rhamnose ratio compared to resting controls. Thirteen of the 26 NSAID users and 4 of the 8 non-users reported GI symptoms. It is concluded that (a) ibuprofen but not aspirin ingestion during prolonged exercise may increase gastrointestinal permeability and lead to GI symptoms, and (b) prolonged exercise alone can produce GI symptoms.

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.

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