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

Male Sprague-Dawley rats were treated ip with beta-naphthoflavone (BNF, 40 mg/kg/day) in dimethylsulfoxide (DMSO, 26.7 mg BNF/ml) for three days. At 24 hr after the pretreatment DMSO (3.0 ml/kg), phenanthrene (150 mg/kg), ozonized or nitrated products of phenanthrene (150 mg/kg), pyrene (150 mg/kg), or ozonized or nitrated products of pyrene (150 mg/kg) were injected ip. Phenanthrene, pyrene, and their ozonized or nitrated products were dissolved in DMSO (50 mg/ml). No increase in the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT) or sorbitol dehydrogenase (SDH) was seen in the pretreated rats 48 hr after the treatment. This is in contrast to what was seen in previous work without the BNF pretreatment. BNF pretreatment induced a small but significant increase in gamma-glutamyl transpeptidase (GGTP) levels. No treatment group receiving BNF differed from another with respect to GGTP. A decrease in lactate dehydrogenase (LDH) levels was noted in the nitro-PAH treatment groups; the same phenomenon was observed earlier in rats treated with nitro-PAH without BNF treatment. These results suggest that the mixed-function oxidase systems specifically induced by BNF have a protective effect against the hepatotoxicity of the oxonized or nitrated products of phenanthrene and pyrene.
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PMID:Toxicity of polycyclic aromatic hydrocarbons. III. Effects of beta-naphthoflavone pretreatment on hepatotoxicity of compounds produced in the ozonation or NO2-nitration of phenanthrene and pyrene in rats. 357 42

Quinidine in vitro significantly reduced accumulation of TEA (tetraethyl ammonium) and PAH (p-amino hippurate) and inhibited oxygen consumption in renal cortical slices. Mitochondrial respiratory control index (RCI) and ADP/O ratio were decreased. Intraperitoneal administration of quinidine at 75 mg/kg twice a day for four days inhibited TEA transport in renal cortical slices and decreased oxygen consumption. Mitochondria showed a reduction in ADP/O ratio but no change in RCI. Serum biochemical measurements indicated a significant elevation in serum creatinine, alanine aminotransferase (ALT), and aspartate aminotransferase (AST).
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PMID:In vitro and in vivo effects of quinidine on the kidneys in Fischer-344 rats. 830 84

The protective effect of N-(2-mercaptopropionyl)-glycine (tiopronin), a clinically used sulfhydryl-containing compound, on cisplatin-induced toxicity to rat renal cortical slices was investigated. Exposure of the slices to cisplatin (2 mM) resulted in toxicity, as shown by an increase in leakage of the two enzymes aspartate aminotransferase and lactate dehydrogenase into the incubation medium and a time-dependent decrease in the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) by the slices. Tiopronin (2 mM) completely prevented the cisplatin-induced increase in enzyme leakage and substantially blocked the decrease of MTT reduction caused by cisplatin. These protective effects were concentration-dependent and furthermore, the depletion of ATP, glutathione and induction of lipid peroxidation in the slices by cisplatin (2 mM) were reversed by 2 mM tiopronin. Pretreatment of slices with tiopronin for 60 min also significantly protected the renal slices from cisplatin-induced toxic effects. These protective effects, however, were abolished by p-aminohippuric acid, a compound with some structural similarity to tiopronin, which both undergoes and inhibits active transport in the cells of the proximal convoluted tubule. Cisplatin (1 mM) also depleted the free sulfhydryls of tiopronin (1 mM) in a second incubation medium system and PAH (2 mM) diminished the extent of this depletion somewhat. These observations suggest that tiopronin protects against cisplatin-induced nephrotoxicity by acting as an alternative target for cisplatin both intra- and extracellularly and thus protects against cisplatin-induced depletion of glutathione in the kidney cell.
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PMID:Tiopronin protects against the nephrotoxicity of cisplatin in rat renal cortical slices in vitro. 897 67