Acrolein produced from polyamines as one of the uraemic toxins

2003 ◽  
Vol 31 (2) ◽  
pp. 371-374 ◽  
Author(s):  
K. Sakata ◽  
K. Kashiwagi ◽  
S. Sharmin ◽  
S. Ueda ◽  
K. Igarashi
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Oxidase Activity ◽  
Culture Medium ◽  
Cellular Proliferation ◽  
Amine Oxidase ◽  
Early Stage ◽  
Chronic Glomerulonephritis ◽  
Toxic Compound ◽  
Amine Oxidase Activity

It is well known that the addition of spermine or spermidine to culture medium containing ruminant serum inhibits cellular proliferation. This effect is caused by the products of oxidation of polyamines that are generated by serum amine oxidase. Among the products, we found that acrolein is a major toxic compound produced from spermine and spermidine by amine oxidase. We then analysed the level of polyamines (putrescine, spermidine and spermine) and amine oxidase activity in plasma of patients with chronic renal failure. It was found that the levels of putrescine and the amine oxidase activity were increased, whereas spermidine and spermine were decreased in plasma of patients with chronic renal failure. The levels of free and protein-conjugated acrolein were also increased in plasma of patients with chronic renal failure. An increase in putrescine, amine oxidase and acrolein in plasma was observed in all cases such as diabetic nephropathy, chronic glomerulonephritis and nephrosclerosis. These results suggest that acrolein is produced during the early stage of nephritis through kidney damage and also during uraemia through accumulation of polyamines in blood due to the decrease in their excretion into urine.

Alteration of serum semicarbazide-sensitive amine oxidase activity in chronic renal failure

2007 ◽  
Vol 114 (6) ◽  
pp. 841-843 ◽  
Author(s):  
J. Nemcsik ◽  
É. Szökö ◽  
Zs. Soltész ◽  
E. Fodor ◽  
L. Toth ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Oxidase Activity ◽  
Amine Oxidase ◽  
Amine Oxidase Activity

Mitochondrial Oxidation of p-N, N-Dimethylamino-β-Phenethylamine (DAPA)

1975 ◽  
Vol 33 ◽  
pp. 458-459
Author(s):  
W. Allen Shannon ◽  
Hannah L. Wasserkrug ◽  
andArnold M. Seligman
Keyword(s):  
Guinea Pig ◽  
Oxidase Activity ◽  
Amine Oxidase ◽  
Histochemical Demonstration ◽  
Guinea Pig Heart ◽  
Pig Kidney ◽  
Cytoplasmic Vacuoles ◽  
Liver And Kidney ◽  
Mitochondrial Oxidation ◽  
Amine Oxidase Activity

The synthesis of a new substrate, p-N,N-dimethylamino-β-phenethylamine (DAPA)3 (Fig. 1) (1,2), and the testing of it as a possible substrate for tissue amine oxidase activity have resulted in the ultracytochemical localization of enzyme oxidase activity referred to as DAPA oxidase (DAPAO). DAPA was designed with the goal of providing an amine that would yield on oxidation a stronger reducing aldehyde than does tryptamine in the histochemical demonstration of monoamine oxidase (MAO) with tetrazolium salts.Ultracytochemical preparations of guinea pig heart, liver and kidney and rat heart and liver were studied. Guinea pig kidney, known to exhibit high levels of MAO, appeared the most reactive of the tissues studied. DAPAO reaction product appears primarily in mitochondrial outer compartments and cristae (Figs. 2-4). Reaction product is also localized in endoplasmic reticulum, cytoplasmic vacuoles and nuclear envelopes (Figs. 2 and 3) and in the sarcoplasmic reticulum of heart.

Autopsy Findings in Patients Treated by Continuous Ambulatory Peritoneal Dialysis (CAPD)

1986 ◽  
Vol 6 (3) ◽  
pp. 130-135 ◽  
Author(s):  
Kostas Sombolos ◽  
Peter McNamee ◽  
Ahmed Mitwalli ◽  
Sol Rabinovich ◽  
Dimitrios G. Oreopoulos
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Causes Of Death ◽  
Coronary Artery Stenosis ◽  
Renal Diseases ◽  
Chronic Glomerulonephritis ◽  
Insulin Dependent ◽  
The Mean ◽  
Organ Changes ◽  
Acquired Cystic Disease

From October 1977 to October 1985, our pathology department did autopsies on 19 patients (14 men, five women) treated by CAPD for four to 55 (mean 29.3) months. Their mean age was 60.2 (range 28–79) years and the primary renal diseases were diabetes mellitus (eight), nephrosclerosis (five), polycystic kidneys (three), chronic glomerulonephritis (one) and chronic renal failure associated with sarcoidosis and congestive cardiomyopathy in two. During the same period, the authors selected as controls 18 autopsied patients (14 men, four women), who had not had chronic renal failure, and these were matched with the CAPD patients for age, sex, longstanding hypertension and insulin-dependent diabetes. Direct causes of death for CAPD patients were cardiovascular incidents (12) infection (5), pancreatitis (1) and lung cancer (1); in controls, the causes were cardiovascular in 11 and infection in two. Thirteen of the CAPD and 12 autopsied controls had coronary artery stenosis equal to or greater than 70%, and affecting one or more arteries. The mean weight of organs in CAPD patients and controls were similar except for kidneys and the spleen; we found the latter weighed more in those on CAPD (p = 0.002). In CAPD patients the most important organ changes were: evidence of myocardial infarction, old or acute, in nine, acquired cystic disease of the kidney in five, and thickening and adhesions of peritoneum in nine and five respectively.

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