Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured serum aspartate transaminase (AST) concentration and serum hepatitis B virus (HBV) DNA concentration in homosexual men with chronic HBV infection and a spectrum of immune deficiency as a result of exposure to human immunodeficiency virus (HIV). Serum AST and HBV DNA concentrations were similar in patients with varying immune function as indicated by in vivo criteria (diagnosis and skin tests reactivity) and in vitro criteria (lymphocyte transformation responses to mitogens and Candida and tetanus antigens) and were unrelated to the number of circulating T cells, suppressor/cytotoxic cells, helper cells, natural killer cells, and the helper:suppressor ratio. Serum AST concentration and indices of cellular immune function were similar in patients with varying HBV replicative activity (high and low HBV DNA concentrations). The observed lack of relationship between serum AST concentration and indices of cellular immune function and HBV replication suggests either that other factors determine the severity of hepatic inflammation in chronic HBV infection, or that currently available tests of cellular immune function and HBV replicative activity do not accurately reflect processes in the liver.
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PMID:Hepatic inflammation, hepatitis B replication, and cellular immune function in homosexual males with chronic hepatitis B and antibody to human immunodeficiency virus. 334 28

Dogs and white rats with experimental tetanus were examined for blood plasma lipids and red cells, their acid resistance, oxygen balance, cytochrome oxidase and aspartate transaminase activity and muscle ultrastructure. The amount of blood plasma lipids was found to be increased, the lipid content in red cells was lowered because of phospholipid washing out. The red cell resistance was lowered, their sedimentation rate was accelerated. Oxygen metabolism in muscles was first enhanced to form excess lipid peroxides, disturbing the integrity of cell membranes and myocyte ultrastructure, and then it was suppressed because of depletion of the compensatory mechanisms and eventuated in the destruction of part of cells and later on in the death of animals.
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PMID:[Changes in lipid metabolism, oxygen balance and muscle ultrastructure in tetanus in an experiment]. 407 63

Seven horses developed clinical or subclinical hepatitis 48 to 87 days after administration of tetanus antitoxin. One horse had mildly high hepatic enzyme activity 120 days after inoculation with tetanus antitoxin. The first horse developed signs of depression, lethargy, and anorexia. During hospitalization, signs of hepatoencephalopathy were noticed, and laboratory data were consistent with hepatic disease. Another horse that was found dead had gross and histologic lesions compatible with serum hepatitis. Screening of serum gamma-glutamyltransferase (GGT) and aspartate transaminase activities were used to investigate the remaining horses in the herd. High GGT activities (71 to 206 IU/L) were detected in 5 additional herd members. These horses appeared clinically normal, apart from 2 reports of nasal photosensitization and an aborted fetus. In 3 horses, high serum GGT activity persisted over a 44-day testing period. All affected horses had been given tetanus antitoxin within 12 hours of parturition, and a common source of vaccine was identified for 7 horses. Findings in this group of horses indicate that clinical and subclinical serum hepatitis can develop after administration of tetanus antitoxin.
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PMID:Hepatic disease associated with administration of tetanus antitoxin in eight horses. 778 47