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glutamic dehydrogenase/fibrosis
L'enllaç es desa al porta-retalls
7 resultats
[Assessment of glutamic dehydrogenase activity in liver cirrhosis].
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Role of oxidative stress and antioxidant therapy in alcoholic and nonalcoholic liver diseases.
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The main pathway for the hepatic oxidation of ethanol to acetaldehyde proceeds via ADH and is associated with the reduction of NAD to NADH; the latter produces a striking redox change with various associated metabolic disorders. NADH also inhibits xanthine dehydrogenase activity, resulting in a
Effects of ethanol consumption on bioactivation and hepatotoxicity of N-nitrosodimethylamine in rats.
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To study the effects of ethanol on the hepatotoxicity of N-nitrosodimethylamine (NDMA), 5 mg NDMA/kg body weight was injected intraperitoneally 3 times a week for 6 weeks into rats pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrates. Another group of rats
Impaired oxygen utilization. A new mechanism for the hepatotoxicity of ethanol in sub-human primates.
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The role of oxygenation in the pathogenesis of alcoholic liver injury was investigated in six baboons fed alcohol chronically and in six pair-fed controls. All animals fed alcohol developed fatty liver with, in addition, fibrosis in three. No evidence for hypoxia was found, both in the basal state
Alcoholism and alcoholic liver injury: new diagnostic and prognostic tests.
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Recently developed tests that measure levels of alpha-amino-n-butyric acid (AANB) and serum glutamic dehydrogenase (GDH) may improve screening for early detection of heavy drinking and liver injury, respectively. With these tests, a "three-level" approach to the problem is now possible: (1)
Blood markers of alcoholic liver disease.
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Not all heavy drinkers develop severe alcoholic liver disease. Genetic factors are probably involved, but no corresponding useful markers have been developed thus far. Of greater practical applicability is the recognition of early changes in the liver that may indicate that the process of scarring
S-Adenosyl-L-methionine and alcoholic liver disease in animal models: implications for early intervention in human beings.
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In patients with severe alcoholic liver disease (i.e., cirrhosis), a deficiency of S-adenosylmethionine (SAMe) develops as a result of decreased SAMe synthetase activity. Whether a sizeable SAMe depletion occurs already at earlier stages of alcoholic liver disease has been the subject of debate. To
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