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 utilized immunoperoxidase methods to study the distribution of both cytosolic or soluble(s) and mitochondrial (m) aspartate aminotransferase (AspAT) in normal, ischemic, and necrotic myocardium. Human myocardium was obtained from autopsy (n = 9) and surgery (n = 6). Cardiac tissue from 26 dogs with experimental myocardial infarction induced by closed-chest balloon occlusion and four dogs with myocardial ischemia without necrosis induced by a 50% reduction in left main coronary artery flow for 3 hours were studied. Duration of occlusion was 45 minutes (n = 1), 3 hours (n = 11), 5 to 6 hours (n = 10), or 15 to 24 hours (n = 4). Highly purified m- and s-AspAT and specific antibodies were prepared in our laboratory. In all cases, control experiments were performed. Microscopically normal human and dog myocardium uniformly stained for m- and s-AspAT. Necrotic myocardium from patients with infarcts showed markedly reduced immunostaining. In those dogs with myocardial necrosis, all dogs with coronary occlusion of 5 to 24 hours, and eight of 11 dogs with 3-hour occlusions, immunostaining was significantly reduced for both s- and m-AspAT in regions confirmed to be necrotic by triphenyl tetrazolium chloride and hematoxylin and eosin staining. Myocardial necrosis was confirmed in the 3-hour infarcts by electron microscopy. In the four dogs with a 50% reduction in left main flow for 3 hours, and one dog with a 45-minute coronary occlusion, ischemia was demonstrated by glycogen loss in period acid-Schiff-stained sections but there was no evidence of necrosis by electron microscopy or triphenyl tetrazolium chloride staining and there was no loss of immunostaining evident for s- or m-AspAT. Thus, s- and m-AspAT were visualized in normal and ischemic myocardium with decreased staining in necrotic tissue using immunoperoxidase techniques. Loss of both s- and m-AspAT can be demonstrated in human myocardium and in experimental canine myocardium as early as 3 hours after coronary occlusion and appears to be specific for irreversible myocardial injury. No depletion of isoenzyme can be detected by immunohistochemical techniques in tissue that is ischemic but not necrotic. Furthermore, by these immunoperoxidase techniques, loss of s- and m-AspAT from necrotic myocardium appears to be simultaneous.
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PMID:Distribution of cytosolic and mitochondrial aspartate aminotransferase in normal, ischemic, and necrotic myocardium. An immunohistochemical study. 638 75

Myocardial necrosis was produced in rats by isoprenaline (ISP) administration (85 mg X kg-1 s.c.) for two consecutive days. Rats sacrificed at 12, 24, 30, 36 and 48 h, respectively, after the last injection of ISP showed a marked increase in serum enzymes, viz. creatine phosphokinase (CPK), lactic dehydrogenase (LDH) and aspartate transaminase (AST) and tissue content of lactate. In addition, there was a significant reduction in the glycogen content of myocardium and the activity of enzyme phosphofructokinase (PFK) was changed in biphasic fashion, i.e. initial enhancement of activity was followed by a persistent fall. All these changes were present along with typical infarct-like necrosis as seen microscopically. Both oxyfedrine (OXF, 2, 4 and 8 mg X kg-1 i.m.) and propranolol (PROP, 1, 2 and 4 mg X kg-1 i.m.) administered for 5 days before and two days during ISP administration were effective in providing protection. However, with 8 mg X kg-1 dose of PROP sporadic high mortality was observed. Serum AST and CPK levels in OXF (4 and 8 mg X kg-1) and PROP (2 and 4 mg X kg-1) pretreated animals returned back to the range of controls. Unlike OXF, the LDH level in PROP pretreated rats, though reduced significantly, remained always higher than the control values. The beneficial effect of OXF on myocardial glycolytic flux was dose-dependent. 8 mg X kg-1 of OXF increased (31%) the glycogen content significantly (p less than 0.01) and the activity of enzyme PFK and tissue lactate content were brought back to normal. PROP did not exhibit dose-dependent reduction in the lactate content of the myocardium and it was never restored back to the range of control values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxyfedrine and propranolol. A comparative experimental approach to protect myocardium against isoprenaline-induced myocardial necrosis. 654 88

Lycopene, a carotenoid rich in tomato fruit (ripe), is an effective antioxidant and free radical scavenger. In this study n-hexane extract of tomato was evaluated for its protective action against oxidative stress in experimental myocardial infarction induced by administration of adrenaline in rats. Adrenaline produced significant elevation of malondialdehyde content of heart, an indicator of lipid peroxidation, with a significant rise in serum aspartate aminotransferase (AST) level and different grades of necrotic changes in myocardium. Rats were treated with two doses of n-hexane extract of tomato, intragastrically daily for one month prior to administration of adrenaline on the 31st and 32nd day. Pretreatment of tomato extract (1 mg/kg, 2 mg/kg) and vitamin E (50 mg/kg) significantly reduced the malondialdehyde concentration in heart and significantly lowered the serum AST level in adrenaline treated rats. Myocardial necrosis was significantly prevented by pretreatment. These results suggest that n-hexane extract of tomato possesses antioxidative property that may protect heart against catecholamine induced myocardial infarction.
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PMID:Protective effect of tomato against adrenaline-induced myocardial infarction in rats. 1947 57