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)

A prospective study was performed in the Dutch flower bulb culture to investigate the possible effects of subchronic exposure to the soil fumigant 1,3-dichloropropene (DCP) on liver and kidney function and on glutathione conjugation capacity in blood. Urine spot samples and venous blood samples from 14 workers applying DCP (applicators) were taken at the start of the season in July, and after the season in October. The parameters of liver function measured were: alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyltranspeptidase, and total bilirubin (conjugated and unconjugated). Total bilirubin was significantly decreased from 9.5 before to 7.0 mumol/l after the season. In combination with an increase in serum gamma-glutamyltranspeptidase activity from 12.5 to 19.5 U/l this indicates moderate hepatic enzyme induction. To study renal function, creatinine and beta 2-microglobulin in serum, and beta 2-microglobulin, albumin, alanine aminopeptidase, beta-galactosidase, and retinol binding protein in urine were measured. The glomerular function parameters albumin in urine and creatinine in serum changed significantly during the season: albumin concentration increased from 5.2 to 7.6 mg/l, whereas creatinine concentration [corrected] decreased from 93.0 to 87.5 mumol/l. The tubular function parameter retinol binding protein also increased in concentration from 20.0 to 26.9 micrograms/l. Therefore, a subclinical nephrotoxic effect of subchronic exposure to DCP cannot be excluded. Effects on glutathione conjugation capacity were studied by measuring erythrocyte glutathione S-transferase activity and blood glutathione concentrations. The activity of glutathione S-transferase in erythrocytes was significantly decreased from 4.7 before to 3.3 U/g haemoglobin after the season. The same was true for the blood glutathione concentrations, which decreased from 0.93 to 0.82 mM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biological effect monitoring of occupational exposure to 1,3-dichloropropene: effects on liver and renal function and on glutathione conjugation. 191 9

We have studied serum and tissue markers of viral replication in 39 patients with chronic hepatitis B virus (HBV) infection and correlated these with periportal and lobular activity in liver biopsies. HBV DNA positivity correlated with the presence of hepatitis B e antigen (HBeAg, P less than 0.001) and aspartate transaminase (AST) levels (P less than 0.005). The lobular but not the periportal inflammatory activity was significantly associated with the presence of HBV DNA (P less than 0.02) and HBeAg (P less than 0.001) and with higher AST levels. The periportal activity correlated with the periportal and lobular display of beta 2-microglobulin on hepatocytes (P less than 0.001 and P less than 0.002, respectively). In patients with chronic HBV infection therefore, the lobular rather than the periportal component of activity was related to viral replication. The association of display of beta 2-microglobulin on hepatocytes with the inflammatory process, in patients with active viral replication, is consistent with the hypothesis that increased display of HLA type I enhances recognition of hepatocytes bearing viral proteins and allows lysis of immune cells.
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PMID:Chronic hepatitis B virus infection. Viral replication and patterns of inflammatory activity: serological, clinical and histological correlations. 354 68

The exposure to organic solvents among 12 graffiti removers was studied. Health effects were also assessed by structured interview and a symptom questionnaire. Blood and urine samples were collected at the end of the day of air sampling. The concentrations of dichloromethane, glycol ethers, trimethylbenzenes and N-methyl-2-pyrrolidinone in the breathing zone of each worker were measured during one working day. The 8-h time-weighted average exposure to dichloromethane ranged from 18 to 1200 mg/m3. The Swedish Permissible Exposure Limit value for dichloromethane is 120 mg/m3. The air concentrations of glycol ethers, trimethylbenzenes and N-methyl-2-pyrrolidinone were low or not detectable. No exposure-related deviations in the serum concentrations of creatinine, aspartate transaminase, alanine transaminase, gamma-glutamyl transpeptidase or hyaluronan or the urine concentrations of alpha 1-microglobulin, beta 2-microglobulin or N-acetyl-beta-glucosaminidase were found. Irritative symptoms of the eyes and upper respiratory tract were more prevalent than in the general population. This study demonstrates that old knowledge about work hazards is not automatically transferred to new professions. Another aspect is that the public is also exposed as the job is performed during daytime in underground stations. At least for short periods, bystanders may be exposed to high concentrations of organic solvent vapours. People with predisposing conditions, e.g. asthmatics, may risk adverse reactions.
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PMID:High exposures to organic solvents among graffiti removers. 814 35

To investigate the theoretic possibility of excessive exposure to thorium during the process of tungsten inert gas (TIG) welding using thoriated rods we carried out a cross-sectional study of TIG welders and an age- and skill-matched group. We measured the radiation doses from inhaled thorium that was retained in the body and investigated whether any differences in health or biologic indices could have been attributable to the welding and tip-grinding process. Sixty-four TIG welders, 11 non-TIG welders, and 61 control subjects from an airline engineering population participated. All of the subjects were interviewed for biographic, occupational history and morbidity details. All of the welders and eight control subjects carried out large-volume urine sampling to recover thorium 232 and thorium 228; this group also had chest radiographs. All of the subjects had a blood sample taken to estimate liver enzymes, and they provided small-volume urine samples for the estimation of retinol-binding protein and beta 2-microglobulin. We found no excess of morbidity among the TIG or non-TIG welding groups, and the levels of retinol-binding protein and beta 2-microglobulin were the same for both groups. There was a higher aspartate aminotransferase level in the control group. The internal radiation doses were estimated at less than an annual level of intake in all cases, and considerably less if the exposure (as was the case) was assumed to be chronic over many years. Some additional precautionary measures are suggested to reduce further any potential hazard from this process.
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PMID:A study of thorium exposure during tungsten inert gas welding in an airline engineering population. 839 74

Pretreatment of fasted rats with aminooxyacetic acid (AOAA, 0.25 mmol kg-1, i.p.), methimazole (MTZ, 0.35 mmol kg-1, i.p.) and acivicin (AT-125, 56 mumol kg-1, i.p.) 30 min prior to a 4-h inhalation exposure to 180-200 ppm or 150-180 ppm vinylidene chloride (VDC) was used to study the role of cysteine beta-lyase, cysteine conjugate S-oxidase and gamma-glutamyltranspeptidase (gamma-GT) in VDC-induced liver and kidney toxicity. Pretreatment with AOAA reduced by 65-95% those increases in serum alanine aminotransferase (ALAT), glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) caused by exposure to 180-200 ppm VDC. This pretreatment also prevented VDC-induced increases in aspartate aminotransferase (ASAT) and N-acetyl-beta-d-glucosaminidase (NAG) activities and in the concentration of beta 2-microglobulin (beta 2-m) in 24-h urine samples. There was only a slight potentiation of VDC-induced liver and renal toxicities by MTZ given before exposure to 180-200 ppm VDC, but potentiation became significant (40-80%) when MTZ was administered before a slightly lower level of exposure (150-180 ppm). Pretreatment with AT-125 did not significantly change the liver and renal effects of exposure to 180-200 ppm VDC. These results suggest that the formation of a cysteine conjugate may be involved in the renal and liver toxicity of VDC in fasted rats.
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PMID:Role of cysteine conjugation in vinylidene chloride-induced nephrotoxicity and hepatotoxicity in fasted rats. 893 83

The two conjugates, S-[N-(2-hydroxyethyl)carbamoylmethyl]glutathione (GSAAE), and its corresponding mercapturic derivative N-acetyl-S-[N-(2-hydroxyethyl)carbamoylmethyl]cysteine (NCySAAE) were administered to fasted Sprague-Dawley rats as putative metabolites of vinylidene chloride (VDC). Methylthioacetylaminoethanol (MAAE) was identified in the urine of GSAAE- or NCySAAE-treated rats (0.5-2.0 mmol/kg, i.p.), as well as in the urine of VDC-treated rats (0.5-2.0 mmol/kg, p.o.). The effects of VDC, GSAAE and NCySAAE on the kidney and liver were also examined using aspartate aminotransferase (ASAT). N-acetyl-beta-D-glucosaminidase (NAG) and beta 2-microglobulin (beta 2-m) as urinary parameters of nephrotoxicity, and glutamate dehydrogenase (GLDH), sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALAT) as serum parameters of hepatotoxicity. Unlike treatment with VDC, treatment with both GSAAE and NCySAAE failed to cause kidney and liver toxicity. The results support the hypothesis that MAAE originates from the formation of GSAAE and further metabolization to NCySAAE, and that MAAE excretion does not reveal a pathway of reactive intermediates.
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PMID:Formation of GSH-derivatives as a pathway for inactive intermediates in vinylidene chloride-treated rats. 900 91

In utero exposure of rats to low levels of the anaesthetic halothane has been reported to produce ultrastructural changes in the liver and kidney at birth. The current study examined the postnatal functional capacities of the liver and the kidney following prenatal exposure to halothane. Halothane or its oxidative metabolite trifluoroacetic acid (TFAA) were given to Sprague-Dawley rats on gestational days 10-20. Halothane was administered by inhalation at concentration of 50 or 500 ppm 6 h-1 day-1, and TFAA was administered by gavage at doses of 75 or 150 mg kg-1 day-1. The exposed offsprings were examined on postnatal days 3, 12 or 49 for hepatic and renal biochemistry and/or function through measurements of several serum and urinary parameters. Neither halothane nor TFAA treatments had statistically significant effect on litter size, neonatal survival or postnatal growth. Both prenatal halothane and TFAA exposure produced changes in liver biochemistry of newborns, as indicated by significant increases in the serum activities of glutamate dehydrogenase and aspartate aminotransferase. In addition, TFAA caused a functional deficit of the proximal tubule in newborns, as evidenced by the significant increase in the urinary excretion of beta 2-microglobulin. However, these hepatic and renal alterations were restricted to the early postnatal period and were no longer observed by postnatal day 49. It is concluded that prenatal exposure to relatively low levels of halothane can cause slight and transient changes in the neonatal rat liver.
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PMID:Postnatal hepatic and renal consequences of in utero exposure to halothane or its oxidative metabolite trifluoroacetic acid in the rat. 904 22