Plasma Enzyme and Isoenzyme Changes during Perfusion of the Isolated Pig Liver

1974 ◽  
Vol 46 (1) ◽  
pp. 105-112
Author(s):  
J. E. Buttery ◽  
S. P. Parbhoo ◽  
D. N. Baron

1. Changes in the perfusate activities of aspartate transaminase, lactate dehydrogenase, its ‘LD-5’ component, sorbitol dehydrogenase, ornithine carbamoyltransferase, and the isoenzyme patterns of lactate dehydrogenase and aspartate transaminase, were investigated in eleven perfusions of pig liver with human blood in order to assess liver cell damage during perfusion. 2. The aspartate transaminase values were a sensitive indicator of liver damage provided that, as was usually the case, the degree of haemolysis was small. Appearance on electrophoresis of the mitochondrial isoenzyme of aspartate transaminase indicated severe liver damage. 3. Measurement of sorbitol dehydrogenase activity was also shown to be a sensitive index of liver cell damage, and had the advantage that haemolysis did not interfere. 4. Measurement of total lactate dehydrogenase activity was unreliable as this largely reflected the degree of haemolysis rather than liver cell damage. However, the isoenzyme pattern of lactate dehydrogenase on electrophoresis distinguished liver cell damage from haemolysis. The chemical determination of ‘LD-5’ was not a sensitive index of pig liver damage as this fraction is found only in low concentration in pig liver. 5. Ornithine carbamoyltransferase was also found not to be a sensitive marker of liver cell damage.

2019 ◽  
Vol 51 (3) ◽  
pp. 134-140
Author(s):  
Diding Heri Prasetyo ◽  
Sarsono Sarsono ◽  
Ida Nurwati ◽  
Prihandjojo Andri Putranto ◽  
Martini Martini ◽  
...  

Liver cirrhosis is the irreversible stage in liver damage process which occurs after liver fibrosis due to necro-inflammatory activities and liver fibrosis. Therefore, inhibition of liver inflammation and fibrosis is very important to prevent liver cirrhosis. This study aimed to analyze the effect of ethanol extract of propolis (EEP) from mount Lawu, Indonesia to prevent liver damage and fibrosis progression in mice with hepatic cirrhosis. This study was performed during the period of June 2018 to May 2019 on a sample of 32 male Balb/C mice divided into control group (P1), induction of carbon tetrachloride (CCl4 ) group (P2), induction of 50 mg/BW CCl4 + EEP group (P3), and (induction of 100 mg/KgBW CCl4 + EEP (P4) with each group consisted of eight mice. The CCl4 in olive oil was administered intraperitoneally three times a week for six weeks. Mean differences between group was determined using ANOVA test with a significance level of 0.05. The induction of CCl4 increased liver cell damage and serum alanin aminotransferase (ALT) level. However, the addition of EEP significantly (p<0.001) reduced liver cell damage as seen in P3 (54.38±4.17 per 100 liver cells) and P4 (37.13±4.36 per 100 liver cells) groups and serum alanin aminotransferase (ALT) as seen in P3 (291.19±113.92 U/L) and P4 (229.38±73.45 U/L) groups. The APRI scores were also reduced after EEP as seen in P3 (0.738±0.292) and P4 (0.513±0.253) groups. Thus, EEP isolates from Gunung Lawu can reduce liver cell damage and fibrosis in mice model of hepatic cirrhosis.


2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Tadashi Nakamura ◽  
Yoshiji Ohta ◽  
Koji Ohashi ◽  
Kumiko Ikeno ◽  
Rie Watanabe ◽  
...  

We examined the protective effect of Brazilian propolis against liver damage with cholestasis in rats treated withα-naphthylisothiocyanate (ANIT) in comparison with that of vitamin E (VE). Rats orally received Brazilian propolis ethanol extract (BPEE) (25, 50, or 100 mg/kg), VE (250 mg/kg) or vehicle at 12 h after intraperitoneal injection of ANIT (75 mg/kg) and were killed 24 h after the injection. Vehicle-treated rats showed liver cell damage and cholestasis, judging from the levels of serum marker enzymes and components. The vehicle group had increased serum total cholesterol, triglyceride, phospholipid, and lipid peroxide levels, increased hepatic lipid peroxide, reduced glutathione, and ascorbic acid levels and myeloperoxidase activity, and decreased hepatic superoxide dismutase activity. BPEE (50 mg/kg) administered to ANIT-treated rats prevented liver cell damage and cholestasis and attenuated these serum and hepatic biochemical changes except hepatic ascorbic acid, although administered BPEE (25 or 100 mg/kg) was less effective. VE administered to ANIT-treated rats prevented liver cell damage, but not cholestasis, and attenuated increased serum lipid peroxide level, increased hepatic lipid peroxide level and myeloperoxidase activity, and decreased hepatic superoxide dismutase activity. These results indicate that BPEE protects against ANIT-induced liver damage with cholestasis in rats more effectively than VE.


1999 ◽  
Vol 11 (9) ◽  
pp. 949-956 ◽  
Author(s):  
Richard K. Thomson ◽  
Michael J. P. Arthur

1986 ◽  
Vol 18 (3) ◽  
pp. 261-276 ◽  
Author(s):  
P. Karayiannis ◽  
T. Jowett ◽  
M. Enticott ◽  
D. Moore ◽  
M. Pignatelli ◽  
...  

1980 ◽  
Vol 58 (4) ◽  
pp. 321-325 ◽  
Author(s):  
F. M. J. Zuyderhoudt ◽  
G. G. A. Jörning ◽  
J. G. De Haan ◽  
G. Samson ◽  
J. Van Gool

1. d-Galactosamine-HCl induces toxic hepatitis in the rat and was used as a model to study some aspects of iron metabolism during liver cell damage. Some changes in iron metabolism were similar to those encountered in human acute viral hepatitis. 2. During the first 3 days of liver cell damage induced by galactosamine, liver depot iron and especially ferritin iron decreased by approximately 20%. Plasma ferritin rose, with a peak mean value which was approximately 20 times the concentration measured in normal rats. 3. During the acute phase, plasma ferritin did not accurately reflect the change in the level of liver depot iron. 4. During and after the acute phase, liver depot iron increased after an initial decrease. The non-ferritin depot iron fraction was elevated approximately 75% compared with the value in normal rats. This increase in non-ferritin iron was probably caused by increased erythrocyte catabolism in the liver and recapture followed by catabolism of liver ferritin that had leaked into the blood.


1987 ◽  
Vol 36 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Hartmut Jaeschke ◽  
Christin Kleinwaechter ◽  
Albrecht Wendel

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