Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatotoxic effects of inorganic mercury with and without pretreatment of phenobarbitone and promethazine have been described in experiments on domesticated rabbits. The total body weight and the relative liver weight decreased after mercury treatment under all experimental conditions. After phenobarbitone (PB) treatment, the serum glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), isocitrate dehydrogenase (ICDH), and lactate dehydrogenase (LDH) activities decreased to 31%, 77%, 20%, and 27%, respectively, whereas the serum alkaline phosphatase (AP) activity increased 54%. After promethazine (PM) treatment, however, the serum GPT activity was inhibited 73%, whereas the serum LDH activity increased 53%. Both hepatic GPT and AP activities decreased after PB (41% and 46%, respectively) and after PM (50% and 52%, respectively) treatments, while the activities of LDH and ICDH increased (after PB: 924% and 108%, respectively; after PM: 147% and 40%, respectively). After mercuric chloride (HgCl2) treatment, the serum GOT, GPT, LDH, and ICDH activities decreased 69%, 83%, 11%, and 48%, respectively. The hepatic GOT, LDH, and AP activities increased 56%, 129%, and 51%, respectively. The administration of HgCl2 in PB-pretreated animals was associated with a decrease in the activities of serum GOT and AP (57% and 69%, respectively), while the ICDH activity increased 27%. The hepatic GOT, GPT, and AP increased 58%, 135%, and 77%, respectively, after mercury treatment, whereas LDH and ICDH were inhibited 78% and 29%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sublethal effects of inorganic mercury on the body growth rate and liver function enzymes of phenobarbitone-pretreated and promethazine-pretreated rabbits. 788 43

The serum immunoglobulin (IgG, IgM and IgA) concentrations of 44 mercury-exposed workers were examined and compared with those of non-exposed, age- and sex-matched individuals. At the time of testing, the exposed population had a mean (+/- S.D.) mercury urinary concentration of 24.7 +/- 19.1 and in 40 of them urinary mercury levels were below the currently accepted limit of 50 micrograms/g creatinine. Increased IgG, IgA and IgM levels were found in the mercury-exposed individuals and in 16, a second evaluation was performed six months later. During the intervening six months, the level of hygiene was improved throughout the plant, and urinary mercury concentrations were determined monthly in each worker. Despite a significant reduction in mercury urinary concentrations, serum immunoglobulin levels did not return to the normal range. There was no correlation between the length or level of exposure and the immunoglobulin levels. Liver protein synthesis, as studied by factor V, prothrombin time, prealbumin and transaminase activity, was normal and liver injury, as evaluated by serum aspartate and alanine aminotransferase activities (AST and ALT, respectively), was not observed. No haematological abnormalities were noted. These results indicate that "safe" levels of mercury exposure may lead to humoral immunological stimulation.
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PMID:Immunoglobulin levels in workers exposed to inorganic mercury. 819 Jul 5

Mercury is the major component of dental amalgam restorative material, which typically has 50% pure elemental mercury. It is also used in some skin creams, and in the manufacturing of plastic, drugs and fungicides. The present study was designed to investigate the toxicity of methyl mercury (MeHg+) on isolated rat hepatocytes using several toxicity parameters. The hepatocytes were isolated by a collagenase perfusion technique and were incubated with different concentrations of MeHg+ (0.1-100 ppm) for 2 h. Through the incubation period the viability was determined by Trypan blue exclusion. Reduced glutathione (GSH) content and its enzymes, glutathione peroxidase (GSH-PX) and glutathione reductase (GSH-RX) were measured. Leakage of enzymes such as aspartate transaminase (AST), and alanine transaminase (ALT) were determined. The cell viability was reduced significantly after 1 h incubation when 0.1 and 1 ppm MeHg+ were applied. The decrease in the cell viability was dose- and time-dependent. A depletion of GSH content was observed with 100 ppm MeHg+ after 30 min of incubation. A significant decrease in GSH-RX was observed with 100 ppm during 15 and 30 min of incubation, while 10 ppm of MeHg+ significantly increased ALT leakage after 60 min. However, there was a significant increase in AST leakage with 100 ppm only. The present investigation indicates that the toxic effect of MeHg+ is most likely cytosolic enzyme related.
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PMID:The mechanism of methyl mercury toxicity in isolated rat hepatocytes. 835 70

Manzala Lake exposed to many pollutants including untreated sewage, agricultural and industrial wastes which increase the concentration of heavy metals, and compromise the health state of the fishermen. This study investigated 100 fishermen and 100 males of other occupations as controls. Both groups work in and live on and around the lake. Clinical examination revealed no significant changes between the fishermen and control group as regards the cardiovascular, gastrointestinal and dermatological systems. However, the urinary, musculoskeletal and respiratory symptoms were significantly higher in fishermen than in control males. There was a significant decrease in neutrophils (48.8%) and a significant increase in lymphocytes and eosinophils (35.4% and 9%), respectively. Hepatotoxicity was evidenced by an increase in serum aspartate transaminase and alanine transaminase. There were no significant differences in serum creatinine and urea between fishermen and control. Levels of lead, cadmium and mercury in water and sediment were 0.26, 0.014, 0.002 mg/l, and 33.5, 1.37, 0.28 micrograms/kg, respectively. Levels of the three heavy metals in the fish samples and serum of fishermen and control males in average were 1.06, 0.18, 0.00025 ppm, 523, 33.5, 13.7 micrograms/l and 374, 12.8 11.2 micrograms/l, respectively. This study aimed to establish the relation between the environmental pollution and the health status of the population inhabiting the contaminated areas.
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PMID:Relationship between environmental pollution in Manzala Lake and health profile of fishermen. 958 78

Laboratory rats were exposed to the inhalation of dust from an agglomeration unit which is the greatest contributor to dust pollution in the vicinity of a mercury producing plant. The exposure lasted for 6 months (4 hours daily, 5 days per week), the concentration of aerosol in the chamber was 10 mg x m(-3). After finishing the exposure, the animals were examined and compared with the controls which were held under standard laboratory conditions. The number of alveolar macrophages was highly elevated (P< 0.001) in the exposed animals, Mg2+ ATPase activity in the heart muscle was decreased. The alanine aminotransferase activity in the serum was not changed, the aspartate aminotransferase was slightly enhanced. No differences in the frequency of abnormal sperm and in the frequency of polychromatic erythrocytes in bone marrow were detected.
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PMID:The chamber exposure of laboratory rats to metal oxides originating from metal producing industry. 972 20

The three-dimensional structure of diaminopelargonic acid synthase, a vitamin B6-dependent enzyme in the pathway of the biosynthesis of biotin, has been determined to 1.8 A resolution by X-ray crystallography. The structure was solved by multi-wavelength anomalous diffraction techniques using a crystal derivatized with mercury ions. The protein model has been refined to a crystallographic R -value of 17.5% (R -free 22.6%). Each enzyme subunit consists of two domains, a large domain (residues 50-329) containing a seven-stranded predominantly parallel beta-sheet, surrounded by alpha-helices, and a small domain comprising residues 1-49 and 330-429. Two subunits, related by a non-crystallographic dyad in the crystals, form the homodimeric molecule, which contains two equal active sites. Pyridoxal-5'-phosphate is bound in a cleft formed by both domains of one subunit and the large domain of the second subunit. The cofactor is anchored to the enzyme by a covalent linkage to the side-chain of the invariant residue Lys274. The phosphate group interacts with main-chain nitrogen atoms and the side-chain of Ser113, located at the N terminus of an alpha-helix. The pyridine nitrogen forms a hydrogen bond to the side-chain of the invariant residue Asp245. Electron density corresponding to a metal ion, most likely Na(+), was found in a tight turn at the surface of the enzyme. Structure analysis reveals that diaminopelargonic acid synthase belongs to the family of vitamin B6-dependent aminotransferases with the same fold as originally observed in aspartate aminotransferase. A multiple structure alignment of enzymes in this family indicated that they form at least six different subclasses. Striking differences in the fold of the N-terminal part of the polypeptide chain are one of the hallmarks of these subclasses. Diaminopelargonic acid synthase is a member of the aminotransferase subclass III. From the structure of the non-productive complex of the holoenzyme with the substrate 7-keto-8-aminopelargonic acid the location of the active site and residues involved in substrate binding have been identified.
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PMID:Crystal structure of diaminopelargonic acid synthase: evolutionary relationships between pyridoxal-5'-phosphate-dependent enzymes. 1045 93

Recent studies have reported on the toxicity and related oxidative stress of selenium and mercury. The present study compares the effects of Se as sodium selenite (Na2SeO3) and Hg as mercuric chloride (HgCl2) separately and in combination. Rats received repeated oral doses of Se (0.5 micromol/ml), Hg (0.5 micromol/ml), or Se in combination with Hg (0.5 micromol/ml of each) for 5 consecutive days. Rat serum, brain and liver samples were collected for biochemical assays. The following biochemical alterations occurred in response to Hg treatment: protein content (brain and liver), acetylcholinesterase (AChE) (brain and serum), acid and alkaline (AcP and AlP) phosphatases (plasma and liver) and glutathione S-transferase (GST) (plasma and liver) activities were significantly (P<0.05) decreased, while lactate dehydrogenase (LDH) (plasma, brain and liver), aspartate and alanine aminotransferase (AST, ALT) (serum and liver) activities were significantly increased. Thiobarbituric acid reactive substances (TBARS) was significantly increased in brain and liver. Effect of Se alone included decreased AcP, AlP and GST (serum and liver) activities. However, LDH (serum, brain and liver) and AST (liver) and TBARS (brain and liver) increased. Selenium in combination with Hg partially or totally alleviated the toxic effects of Hg on different studied enzymes. It is concluded that Se could be able to antagonize the toxic effects of mercury.
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PMID:Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. 1149 25

HgCl2 (5.0 mg/kg body weight) induced toxicity led to significant elevation of lipid peroxidation (LPO) level but decline in the glutathione content in liver of Swiss albino mice. In serum of HgCl2 treated mice there was significant elevation in serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) activities but significant decline in the alkaline phosphatase activity. Animals treated with O. sanctum extract (10 mg/kg body weight, po) before and after mercury intoxication showed a significant decrease in LPO level, SGOT and SGPT activities and increase in serum alkaline phosphatase activity and glutathione (GSH) content. Ocimum treatment alone did not alter SGOT, SGPT and alkaline phosphatase activities but significantly enhanced reduced glutathione. The results suggest that oral administration of Ocimum extract provides protection against HgCl2 induced toxicity in Swiss albino mice.
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PMID:Ocimum sanctum aqueous leaf extract provides protection against mercury induced toxicity in Swiss albino mice. 1258 43

Mercury is a highly toxic metal which induces oxidative stress. Metallothionein and heat shock protein 70 (HSP70) are stress proteins involved in response to different stimuli. In the present study rats were administered per oral application by gavage, a single daily dose (0.1 mg/kg) of HgCl(2) for 3 consecutive days. To find a relation between these two stress proteins and mercury, parameters of liver injury, redox state of the cells, and the expression and protein levels of HSP70 and metallothionein by Northern and Western blot analysis were assayed either in blood or in liver. HgCl(2) at the doses of 0.1 mg/kg induced liver injury detected by a slight increase in serum aspartate aminotransferase and alkaline phosphatase activities and by the enhanced levels of bilirubin. Oxidative stress was detected by a significant decrease in protein-SH and an increase in thiobarbituric acid reactive substances in liver following one dose of mercury. mRNA and protein levels of both metallothionein and HSP70 increased progressively from first to third doses of mercury. We conclude that against low doses of mercury that produce a slight liver injury and oxidative stress, the liver rapidly responds by inducing the expression of metallothionein and HSP70. We suggest that metallothionein induction attenuates the decrease in protein-SH induced by the first dose of mercury, since metallothionein increases the pool of thiol groups in the cytosol eliminating oxygen radicals and inhibiting lipid peroxidation. From these results we can suggest that the changes observed in these stress proteins by the effect of mercury appear to be a response rapidly induced at transcriptional and at translational levels.
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PMID:Relationship between expression of HSP70 and metallothionein and oxidative stress during mercury chloride induced acute liver injury in rats. 1281 12

Mercury is a well-recognized health hazard and an environmental contaminant. Mercury modulates immune responses ranging from immune suppression to autoimmunity but the mechanisms responsible for these effects are still unclear. Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm mercury in drinking water for 14 days. Body weight was reduced at the highest dose of mercury whereas the relative kidney and spleen weights were significantly increased. The dose range of mercury used did not cause hepatotoxicity as indicated by circulating alanine aminotransferase and aspartate aminotransferase levels. Circulating blood leukocytes were elevated in mice treated with the highest dose of mercury. Mercury ranging from 1.5 to 37.5 ppm dose-dependently decreased CD3(+) T lymphocytes in spleen; both CD4(+) and CD8(+) single-positive lymphocyte populations were decreased. Exposure to 7.5 and 37.5 ppm mercury decreased the CD8(+) T lymphocyte population in the thymus, whereas double-positive CD4(+)/CD8(+) and CD4(+) thymocytes were not altered. Mercury altered the expression of inflammatory cytokines (tumor necrosis factor alpha, interferon gamma, and interleukin-12), c-myc, and major histocompatibility complex II, in various organs. Results indicated that a decrease in T lymphocyte populations in immune organs and altered cytokine gene expression may contribute to the immunotoxic effects of inorganic mercury.
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PMID:Oral exposure to inorganic mercury alters T lymphocyte phenotypes and cytokine expression in BALB/c mice. 1292 68


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