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)

Dietary boron, in amounts usually found in human diets comprised mainly of fruits and vegetables, apparently affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 micrograms B/g and no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of energy metabolism. In the non-STZ rats, supplemental dietary boron substantially depressed plasma insulin, plasma pyruvate concentrations, and creatine kinase activity and increased plasma thyroxine (T4) concentrations. The finding that boron did not affect growth, but did affect several indices of energy metabolism in the non-STZ animals suggests that boron functions as a regulator of energy metabolism in the rat. A decrease in plasma aspartate transaminase activity (an indicator of enhanced cell membrane integrity) in the non-STZ rats suggests that boron exerts a protective influence over normal liver metabolism.
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PMID:Boron affects energy metabolism in the streptozotocin-injected, vitamin D3-deprived rat. 166 21

Following acute accidental death of 26 cows exposed to boron fertilizer, effects of inorganic boron treatment in goats were studied. Goats were orally dosed with toxic but sublethal amounts of the fertilizer. Multiple hematologic and serum chemistry parameters were assessed, as were cerebrospinal fluid (CSF) neurotransmitters and some of their metabolites. Significant increases in packed cell volume, hemoglobin, inorganic phosphate, creatine phosphokinase, conjugated bilirubin, sodium, glucose, cholesterol, and aspartate transaminase were recorded. The following serum components were significantly decreased after boron dosing: alkaline phosphatase, magnesium, glutamyltransferase and potassium. There was evidence of a stimulatory effect on both serotonergic and dopaminergic neurons as reflected in elevated CSF monoamine metabolites. Aberrations in clinical behavior, including seizure-like activity, also suggested a central nervous system effect of inorganic boron.
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PMID:Experimental acute inorganic boron toxicosis in the goat: effects on serum chemistry and CSF biogenic amines. 216 93

Copper tetracarboranyltetraphenylporphyrin (CuTCPH) is a minimally toxic carborane-containing porphyrin that has safely delivered high concentrations of boron for experimental boron neutron capture therapy (BNCT). Copper octabromotetracarboranylphenylporphyrin (CuTCPBr), synthesized by bromination of CuTCPH, is one of several new minimally toxic analogues of CuTCPH being studied in our laboratory, which could possess comparable or better tumour-targeting properties with enhanced tumour cytotoxicity. Its biodistribution, biokinetics and toxicity in mice with subcutaneous EMT-6 (mammary) or SCCVII (squamous cell) carcinomas were compared with those of CuTCPH. The administration of approximately 200 mg kg(-1) of either porphyrin in six intraperitoneal injections over 2 days had no apparent effect, but administration of approximately 400 mg kg(-1) slightly lowered body weights, elevated alanine and aspartate transaminase activities in blood plasma, and depressed blood platelet counts for several days. Enzymes and platelets returned to normal within 5 days after those injections and body weights returned to normal within 2 weeks. High average concentrations of boron from either porphyrin were achieved in the two tumour models from a total dose of approximately 200 mg kg(-1). The high tumour boron concentration decreased slowly while concentrations in blood decreased rapidly. Boron concentrations in brain and skin were consistently lower than in tumour by a factor of 10 or more. Although either CuTCPH or CuTCPBr can be labelled with (64)Cu for imaging by positron emission tomography (PET), CuTCPBr can also be labelled by (76)Br, another PET-imageable nuclide.
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PMID:Synthesis of copper octabromotetracarboranylphenylporphyrin for boron neutron capture therapy and its toxicity and biodistribution in tumour-bearing mice. 1523 4

The influence of dietary boron (B) supplementation on some serum parameters and egg-yolk cholesterol was studied in laying hens. A total of 224 eighteen-week-old hens of the Hyline Brown 98 strain were assigned to 7 groups with 4 replicates of 8 hens each after 10 days of adaptation, and they were fed commercial diets supplemented with 0, 5, 10, 50, 100, 200 or 400 mg/kg (diet) B (H3BO3) for 8 weeks. Serum gamma-glutamyl transpeptidase (GGT) activity, albumin, glucose, total cholesterol, HDL- and LDL-cholesterol levels were decreased with all B levels. Except in the group receiving 5 mg/kg B supplementation, decreases were found in serum triglycerides in all groups. Serum aspartate aminotransferase (AST) activity was decreased in the groups receiving 100 mg/kg or higher levels of B. All levels of B supplementation increased lactate dehydrogenase (LDH) activity at weeks 21 and 22, while 10 mg/kg or higher levels of B increased serum globulin, urea and egg-yolk cholesterol levels. The results demonstrate that B supplementation at levels exceeding 5 mg/kg affects serum biochemical parameters and increases egg-yolk cholesterol in laying hens.
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PMID:Influence of dietary boron supplementation on some serum metabolites and egg-yolk cholesterol in laying hens. 1738 54

Licorice is commonly used as a cure for digestive disorders and as a detoxification agent in East Asia. This study investigated the protective effect of licorice water extract against cadmium (CdCl(2), Cd)-induced liver toxicity in rats. To induce acute toxicity, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously (i.v.) injected into rats. The rats then received either a vehicle or licorice water extract (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd 24 h after the last licorice/vehicle treatment. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with licorice reduced ALT, AST and LDH. In histopathological analysis, licorice decreased the central necrosis around central veins, the peripheral hemorrhage around portal triads, the percentage of degenerative hepatic regions (%/mm(2) hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cells). Licorice also inhibited the increment of Bad (a BH3 domain-containing protein) translocation by Cd in liver cells. These results demonstrate that licorice could have a hepatoprotective effect by inhibiting the translocation of Bad to the mitochondria in Cd-intoxificated rats.
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PMID:Hepatoprotective Activity of Licorice Water Extract against Cadmium-induced Toxicity in Rats. 1895 29

Acuteliver failure (ALF) has a high mortality rate and is characterized by massive hepatocyte destruction. Although microRNAs (miRNAs) play an important role in manyliver diseases, the role of miRNAs in ALF development is unknown. In this study, the murine ALF model was induced by intraperitoneal injection of D-galactosamine/lipopolysaccharide (D-GalN/LPS). Compared with saline-treated mice, miR-24 was distinctly down-regulated post D-GalN/LPS challenge in vivo and D-galactosamine/tumor necrosis factor (D-GalN/TNF) challenge in vitro, which was confirmed by quantitative real-time polymerase chain reaction. Meanwhile, the mRNA and protein levels of the BH3-only-domain-containing protein BIM were upregulated after challenge both in vivo and in vitro. Previous studies have demonstrated that hepatocyte apoptosis is a distinguishing feature of D-GalN/LPS-associated liver failure. In this study, D-GalN/LPS-challenged mice showed higher alanine aminotransferase and aspartate aminotransferase levels, more severe liver damage, increased numbers of apoptotic hepatocytes and higher levels of caspase-3 compared with saline-treated mice. In D-GalN/TNF-treated BNLCL2 cells, miR-24 overexpression attenuated apoptosis.Furthermore, miR-24 overexpression reduced BIM mRNA and protein levels in vitro. Taken together, these findings demonstrate that miR-24 regulates hepatocyte apoptosis via BIM during ALF development, suggesting that miR-24 is a novel onco-miRNA that may provide potential therapeutic targets for ALF.
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PMID:Mir-24 regulates hepatocyte apoptosis via BIM during acute liver failure. 2921 90