Plasma pharmacokinetics and urinary excretion of the polyamine analogue 1, 19-bis(ethylamino)-5, 10, 15-triazanonadecane in CD 2 F 1 mice

1996 ◽  
Vol 38 (1) ◽  
pp. 13-20 ◽  
Author(s):  
J. L. Eiseman ◽  
Zhi-Min Yuan ◽  
Natalie D. Eddington ◽  
Dorothy L. Sentz ◽  
Patrick S. Callery ◽  
...  

2016 ◽  
Vol 358 (2) ◽  
pp. 230-238 ◽  
Author(s):  
A. R. Masters ◽  
B. T. Gufford ◽  
J. B. L. Lu ◽  
I. F. Metzger ◽  
D. R. Jones ◽  
...  


2020 ◽  
Vol 97 ◽  
pp. 365-370
Author(s):  
Tim R. Cressey ◽  
Oraphan Siriprakaisil ◽  
Rachel W. Kubiak ◽  
Virat Klinbuayaem ◽  
Pra-ornsuda Sukrakanchana ◽  
...  


2009 ◽  
Vol 89 (6) ◽  
pp. 1784-1791 ◽  
Author(s):  
William Mullen ◽  
Gina Borges ◽  
Jennifer L Donovan ◽  
Christine A Edwards ◽  
Mauro Serafini ◽  
...  


2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada

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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