Disease relevance of L-aspartate

• The children receiving PN fell into two subgroups: 5 with severe PN-associated cholestatic liver disease (bilirubin level, > 100 mumol/L; aspartate aminotransferase [AST] level, > 200 U/L) and 24 with a bilirubin level of < 100 mumol/L and/or AST level of < 200 U/L [1].
• The efficacy of UDCA in lowering serum AST and ALT was more pronounced in the presence of cirrhosis [2].
• In patients with CHC and ESRD, the presence of stage III-IV fibrosis was significantly associated with hepatic steatosis (OR = 4.523, p= 0.012) and thrombocytopenia (OR = 4.884, p= 0.044), which were independent of the frequencies of a history of DM, splenomegaly, and a higher level of AST [3].
• CONCLUSIONS: In patients with chronic hepatitis C, 23.0% had elevated serum AFP that is independently associated with stage III/IV hepatic fibrosis, elevated level of AST, and prolonged INR [4].
• Hindlimb I/R (IR vs SHAM) resulted in both significant pulmonary neutrophil infiltration (MPO 16.4 +/- 1.06 U/g vs 11.3 +/- 1.4 U/g) and hepatocellular injury (AST 286 +/- 45 U/mL vs 108 +/- 30 U/mL), but neither was inhibited by pretreatment with STNFRI before ischemia [5].

High impact information on L-aspartate

• The amount of blood loss, measurements of liver enzymes alanine aminotransferase (ALT), aspartate aminotransferase (AST), and postoperative evolution were also recorded [6].
• Mutagenesis of aspartate residues Asp84 and 86 to asparagine within this beta-hairpin showed the carboxylate moiety of both residues was required for catalysis but not for dUTP binding [7].
• Redissolved, lyophilized cell extracts were analyzed by 13C nuclear magnetic resonance spectroscopy to investigate neuronal metabolism of lactate and by HPLC for determination of the total amounts of glutamate (Glu), gamma-aminobutyric acid (GABA), and aspartate (Asp) [8].
• Children requiring LT had higher aspartate aminotransferase (AST) at presentation (p<0.0001) and both higher AST and gamma-glutamyl transferase (GGT) at 6 months (p<0.001), 1-year (p<0.0003) and 5-year (p<0.01) follow up when compared to those who are well without LT [9].
• To identify side chains in this peptide that potentially contribute hydrogen bonding or catalytic determinants for the RNA-dependent step of the aminoacylation reaction, peptide functional side chains that are conserved among sequenced alanine enzymes (Asp, Asn, Arg, Glu, Gln, and Tyr) were individually replaced [10].

Chemical compound and disease context of L-aspartate

• Commonly collected clinical data included age, gender, serum aminotransferase (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) and hepatitis B virus (HBV) DNA levels, and IFN-alpha dose [11].
• RESULTS: We found that GLPG can alleviate the L-02 liver cells injury induced by carbon tetrachloride (CCl4) through the measurements of ALT and AST activities and the administration of GLPG to L-02 cells did not display any toxicity [12].
• Endotoxemia for 6 hr resulted in a 5.9-fold rise in the serum levels of nitrite (P < 0.05) with a significant rise in the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactic dehydrogenase (LDH), suggestive of liver dysfunction [13].

Biological context of L-aspartate

• Cell death was assayed via aspartate aminotransferase (AST) release, both immediately following a 2-h oxygen +/- anesthetic exposure and 6 h post-exposure [14].
• OBJECTIVES: To determine the overall incidence of isoniazid (INH) hepatotoxicity in a public health tuberculosis clinic over a 7-year period, and to determine if systematic, limited aspartate aminotransferase (AST) monitoring would be of benefit in detecting INH hepatotoxicity [15].
• Measurements were made of fluoride concentrations in serum, liver and urine (indicators of biotransformation of enflurane), paracetamol concentrations in urine, pathological changes in liver samples, and concentrations of the enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum [16].
• Routinely, hepatocellular damage is diagnosed by, for example, abnormal aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and the prothrombin time (PT) [17].
• Fibrosis and hepatic damage, as reveled by histology and the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were induced in rats by an administration of CCl(4) (8%, 1 ml/kg body weight) thrice a week for 4 weeks [18].

Anatomical context of L-aspartate

• Because skeletal muscle contains more CK and less aspartate aminotransferase (AST) than cardiac muscle, the CK/AST ratio might provide a useful adjunct in evaluating the source of a supranormal value for CK [19].
• The use of trehalose as an additive for cryopreserving human hepatocytes resulted in a significantly increased total protein level in the attached cells, higher secretion of albumin and a lower aspartate aminotransferase (AST) level after thawing [20].
• Pulmonary neutrophil infiltration and hepatocellular injury were assessed by means of myeloperoxidase content (MPO) and aspartate aminotransferase (AST) concentrations, respectively [5].
• Kindling increased ALP activity throughout the brain, elevated AST as well as LDH activity in the frontal cortex and hippocampus and decreased CK activity in the frontal cortex and cerebellum [21].
• The effects of low (10 microg/kg b.w.) and high (100 microg/kg b.w.) doses of mycotoxin-zearalenone on selected blood serum enzyme activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), and total lactatedehydrogenase (LD) of rabbits were studied [22].

Associations of L-aspartate with other chemical compounds

• CONCLUSIONS: With these statistical considerations, we conclude that there was probably no statistically significant difference between the groups for an increase in AST or AP levels during total parenteral nutrition [23].
• Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were not changed in animals exposed to 1-NN but were increased by m-xylene coexposure [24].
• DOX-induced cardiotoxicity was manifested by abnormal biochemical changes including marked increases in serum creatine phosphokinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), and aspartate aminotransferase (AST) activity levels [25].
• The combined regimen elevated plasma homocysteine, hepatic S-adenosylhomocysteine (SAH), urinary 8-hydroxy-2-deoxyguanosine (oxy(8)dG), an index of DNA oxidation, and serum aspartate aminotransferase (AST) levels [26].
• Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), as indexes of hepatic cell disruption, were reduced with puerarin treatment, whereas no significant effect was discovered in the levels of alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT) activities [27].

Gene context of L-aspartate

• Interestingly, Fas-deficient C57BL/6 lpr/lpr mice also showed significant AST levels in the serum following LSA tumor growth [28].
• Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group [29].
• At the end of the follow-up period, significant differences were seen in ALT, aspartate (AST), and iron ferritin and transferrin levels [30].
• Her ALT, AST, GGT, and alkaline phosphatase again increased to 269, 49, 256, and 263 U/L, respectively, 6 days after resuming therapy [31].
• Stratified according to alcohol intake, in moderate drinkers, a positive correlation was found between AN and TNF-alpha concentrations (r = 0.6, p = 0.0001, AST/ALT index (r = 0.34, p = 0.0295) whereas in non-drinkers no such correlations were found [32].

Analytical, diagnostic and therapeutic context of L-aspartate

• Serum AST levels in the NS group increased 120 min after reperfusion, but this change was significantly (P<0.05) reduced in the FR group [33].
• Plasma ALT and AST activities were significantly elevated by CCl4 as early as 3 h after treatment, while the activities in the CHCl3-treated rats did not increase until 6 h after treatment [34].
• CK values correlated with aspartate aminotransferase (AST), erythrocyte sedimentation rate (ESR), body mass index (BMI) and platelets (Plat) in RA; ESR and haemoglobin (Hb) in SLE, AST, ESR and Hb in SpA; lactate dehydrogenase (LDH), AST, ESR and Hb in Poly; LDH, AST, ESR, Hb and Ccr in MI; and LDH, AST and ESR in controls [35].

References