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EXPERIMENTAL LIVER NECROSIS; II. ENZYMES
1Bender Laboratory, Albany, N. Y.
The Journal of Experimental Medicine
|October 30, 2009
Summary
Blood serum inhibits liver autolysis, especially in necrotic tissue. Necrotic livers show increased non-coagulable nitrogen and ammonia production, with arginase absent and tyrosin present in diffuse necrosis.
Area of Science:
- Biochemistry
- Pathology
Background:
- Autolysis, the self-digestion of cells, is a critical process in tissue degradation.
- Liver necrosis involves significant biochemical alterations, impacting protein breakdown and nitrogen metabolism.
Purpose of the Study:
- To investigate the effect of blood serum on liver autolysis in normal and necrotic conditions.
- To analyze the changes in non-coagulable nitrogen, monamino-acids, ammonia production, and specific enzyme/amino acid presence during liver autolysis.
Main Methods:
- Comparison of autolytic rates and nitrogenous compound levels in washed versus unwashed normal and necrotic liver tissues.
- Analysis of ammonia production through partition experiments and absolute production measurements.
- Enzyme assays for arginase and examination of amino acid profiles (leucin, tyrosin) in liver and urine.
Main Results:
- Blood serum significantly inhibits autolysis in both normal and necrotic livers, reducing non-coagulable nitrogen increase.
- Necrotic livers exhibit higher initial and final levels of non-coagulable nitrogen and increased ammonia production compared to normal livers.
- Arginase is absent in necrotic livers, while tyrosin is consistently found in livers with diffuse necrosis and sometimes in urine.
Conclusions:
- Blood serum plays a crucial inhibitory role in liver autolysis.
- Liver necrosis is characterized by accelerated protein breakdown, evidenced by elevated non-coagulable nitrogen and ammonia.
- The absence of arginase and presence of tyrosin in necrotic livers suggest specific metabolic derangements during necrosis.
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