Correlation between X-prolyl dipeptidyl-aminopeptidase and serum amine oxidase in serum of patients with post-burn keloids.

1979 ◽  
Vol 25 (3) ◽  
pp. 376-378 ◽  
Author(s):  
T Nagatsu ◽  
K Iwase ◽  
Y Kasahara ◽  
K Kubono ◽  
S Sakakibara ◽  
...  

Abstract Activities of X-prolyl dipeptidyl-aminopeptidase (EC 3.4.14.1) and amine oxidase (EC 1.4.3.6) in serum were assayed in two groups of patients, children two to nine years old and adults 23 to 60 years old, with hypertrophic scars after severe burn. The peptidase activity tended to be low initially for several months after the burn, but then returned to normal after six months. These changes were marked in the child group, less so in the adult group. Similar but less-pronounced changes were also observed in serum amino oxidase activity. The two serum enzyme activities showed a significant positive correlation (r = 0.668, p less than 0.001, n = 27) in the patients.

Heart ◽  
1970 ◽  
Vol 32 (5) ◽  
pp. 600-602 ◽  
Author(s):  
T. Mandecki ◽  
L. Giec ◽  
W. Kargul

2009 ◽  
Vol 8 (7) ◽  
pp. 700-705 ◽  
Author(s):  
S.F. Hassaan ◽  
S.A. Abdel-Fatt ◽  
A.E. Elsalmoney ◽  
M.S.H. Hassan

1971 ◽  
Vol 47 (2) ◽  
pp. 132-136 ◽  
Author(s):  
JOHN E. HOOPES ◽  
CHI-TSUNG SU ◽  
MICHAEL J. C. IM

1974 ◽  
Vol 47 (5) ◽  
pp. 449-459 ◽  
Author(s):  
B. E. Walker ◽  
J. Kelleher ◽  
M. F. Dixon ◽  
M. S. Losowsky

1. Control, vitamin E-deficient, vitamin E-supplemented (deficient with added ‘normal’ intake) and vitamin E-treated rats were given paracetamol at a dose of 25.5 mmol (4 g)/kg body weight. Control rats were also given paracetamol with or without simultaneous vitamin E. 2. Plasma aspartate aminotransferase and alanine aminotransferase activities increased to very high values (mean 2842 and 1241 i.u./l respectively) in the control group, and even higher (mean 8220 and 2320 i.u./l respectively) in the vitamin E-deficient group. 3. In the vitamin E-supplemented group the rises in activity were similar but rather less than in the control group (mean 2417 and 815 i.u./l) and in the vitamin E-treated group only very small rises (mean 177 and 98 i.u./l) were seen. 4. Histological evidence of hepatic necrosis correlated closely with plasma enzyme activities. 5. It appears that paracetamol-induced hepatic necrosis is potentiated in vitamin E deficiency and reduced by prior treatment with α-tocopherol. 6. Vitamin E administered simultaneously with paracetamol at 12.8 or 19.2 mmol/kg also greatly reduced the expected rise in serum enzyme activities. 7. These observations may shed some light on the mechanism of paracetamol-induced hepatic necrosis, and may form a basis for preventing or reducing this lesion in man.


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