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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the influence of exposure time and concentration on the accumulation of cadmium and the occurrence of adverse effects was investigated when carp were simultaneously exposed through contaminated water and food. As exposure concentrations increased (9, 105, and 480 microg/L through water and 9.5, 122, and 141 microg/g dry weight through food) the accumulation pattern of cadmium changed, with progressively more cadmium being accumulated in the liver and especially the kidney and less in the gills and the intestine. A strong concentration- and time-dependent effect of cadmium exposure on plasma calcium concentrations was observed, leading to a decrease, with approximately 16% in the mid group and up to 50% in the group exposed to the highest cadmium concentration. Also at the highest exposure concentrations, sodium and chloride levels as well as plasma osmolality were significantly reduced, indicating a disturbed ion homeostasis. Furthermore, an increase in plasma alanine transaminase activity indicated liver damage caused by the cadmium accumulation in this organ. At the end of the experiment, general stress responses such as decreased hematocrit, growth, and mortality (17%) also were observed. All together, these results suggest that plasma hypocalcemia as an ion-disruptive phenomenon is the most sensitive effect during cadmium exposure, although the occurrence and magnitude both depend on exposure time and concentration.
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PMID:Dynamics of cadmium accumulation and effects in common carp (Cyprinus carpio) during simultaneous exposure to water and food (Tubifex tubifex). 1676 74

The present study was carried out to assess the endocrine status and liver function in adult cows reared in polluted environment around different industrial units in India. The effect on endocrine system was examined by determination of plasma level of thyroid hormones, thyroxin (T4) (n=269) and triidothyronin (T3) (n=269), stress hormone cortisol (n=266), and reproductive hormones such as estradiol (n=84) and progesterone (n=84) in cows (>3 years) reared around different polluted industrial and non-polluted areas. The respective blood lead and cadmium concentration was also determined in all the cows. The mean plasma levels of both T3 and T4 were significantly (P<0.05) higher around lead zinc smelter (2.43+/-0.26 and 41.1+/-2.9nmol/L) and closed lead cum operational zinc smelter (1.81+/-0.16 and 42.4+/-6.2nmol/L), where the mean blood lead level (0.86+/-0.06 and 0.51+/-0.09mug/ml) was also significantly higher than that of cows (0.07+/-0.01mug/ml) from unpolluted areas. Regression analysis of data from 269 cows revealed a significant (P<0.01) positive correlation between the blood lead and plasma T3 (r=0.287) and T4 (r=0.173). The correlation between thyroidal hormones and the blood cadmium concentration (r=-0.079 and -0.48; P>0.05) was not significant. Plasma cortisol level had also a non-significant (P>0.05) correlation (r=-0.092) with blood lead level.However, the mean cortisol level (4.02+/-1.96nmol/L) of cows in phosphate rock mining areas was significantly (P<0.05) higher than that of controls (1.98+/-0.70nmol/L). The mean plasma estradiol level was significantly (P<0.05) higher in cows around closed lead cum operational zinc smelter (47.1+/-19.5pg/ml) than that of the control animals (21.8+/-3.9pg/ml) and in rest of the areas, the difference did not reach the statistical significance (P>0.05). The serum biochemical analysis in 36 cows around lead-zinc smelter with the highest mean blood lead level (0.86+/-0.06mug/ml) amongst all the industrial/urban areas surveyed, and in 15 animals from non-polluted areas revealed a significant positive correlation between blood lead and serum ALT (alanine transaminase) (r=0.688, P<0.01) and AST (aspartate transaminase) (r=0.390, P<0.01) and a negative correlation with serum total lipids (r=-0.337, P<0.05), total protein (r=-0.449, P<0.01) and albumin(r=-0.662, P<0.01). It is concluded from the study that the natural exposure to lead in polluted environments disturbs the endocrine profile and the higher blood lead level alters serum biochemical parameters indicative of liver functions.
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PMID:Changes in plasma hormones profile and liver function in cows naturally exposed to lead and cadmium around different industrial areas. 1682 33

Gene expression changes in carp liver tissue were studied after acute (3 and 24h) and subchronic (7 and 28 days) exposure to a mixture of waterborne (9, 105 and 480 microg/l) and dietary (9.5, 122 and 144 microg/g) cadmium, using a custom-made microarray. Suppression subtractive hybridization-PCR (SSH-PCR) was applied to isolate a set of 643 liver genes, involved in multiple biological pathways, such as energy metabolism (e.g. glucokinase), immune response (e.g. complement C3) and stress and detoxification (e.g. cytochrome P450 2F2, glutathione-S-transferase pi). These genes were subsequently spotted on glass-slides for the construction of a custom-made microarray. Resulting microarray hybridizations indicated a highly dynamic response to cadmium exposure. At low exposure concentrations (9 microg/l through water and 9.5 microg/g dry weight through food) mostly energy-related genes (e.g. glucokinase, elastase) were influenced, while a general stress response was obvious through induction of several stress-related genes, including hemopexin and cytochrome P450 2F2, at high cadmium concentrations. In addition, fish exposed to the highest cadmium concentrations showed liver damage after 7 days of exposure, as measured by elevated alanine transaminase activity in plasma and increased liver water content (wet-to-dry weight ratio). Moreover, decreased hematocrit and growth were found at the end of the experiment. Altogether this study clearly demonstrated the importance of varying exposure conditions for the characterization of the molecular impact of cadmium and showed that microarray results can provide important information, required to unravel the molecular events and responses related to cadmium exposure.
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PMID:Patterns of gene expression in carp liver after exposure to a mixture of waterborne and dietary cadmium using a custom-made microarray. 1702 62

Metallothionein (MT) is a cysteine-rich protein that binds to and is inducible by heavy metals such as cadmium and zinc. However, the precise mechanism of MT induction by other metals remains unclear. In the present study, we investigated the mechanism of MT induction by manganese, focusing on the involvement of cytokine production. Administration of MnCl(2) to mice resulted in the induction of MT dose-dependently in the liver with little accumulation of manganese. Speciation analysis of metals in the liver cytosol showed that the major metal bound to the induced MT was zinc. Administration of MnCl(2) caused an increase in mRNA levels of interleukin-6 (IL-6) in the liver as well as an increase in serum levels of IL-6 but not those of other inflammatory cytokines. Subsequently, serum levels of serum amyloid A (SAA), an acute-phase protein induced by IL-6, increased with a peak at 24 h. However, no increase in serum alanine aminotransferase activity was observed, suggesting that manganese enhanced the production of IL-6 and SAA without causing liver injury. In response to IL-6, the expression of a zinc transporter, ZIP14, was enhanced in the liver, possibly contributing to the synthesis of hepatic zinc-MT. In IL-6-null mice, the induction of hepatic MT by treatment with MnCl(2) was completely suppressed to the control level. These results suggest that manganese is a unique metal that induces the synthesis of hepatic MT completely depending on the production of IL-6 without accompanying liver injury.
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PMID:Induction of metallothionein by manganese is completely dependent on interleukin-6 production. 1706 64

The therapeutic efficacy of Picroliv--a standardized extract of Picrorhiza kurroa--was investigated in male rats exposed to CdCl2 (0.5 mg/kg, sc), 5 days/week for 18 weeks. Picroliv at two doses (6 and 12 mg/kg, po) was given to the cadmium (Cd)-administered group for the last 4 weeks (i.e., weeks 15-18). The Cd altered oxidative stress indices, such as increased lipid peroxidation and membrane fluidity, reduced levels of non-protein sulphydryls (NPSHs), and Na+K+ATPase activity in the liver and kidney were found close to the control values by Picroliv treatment, suggesting its antioxidant potential. The hepatoprotective action of Picroliv was evident by its ability to lower the Cd-induced liver function parameters--the serum enzymes, such as alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT) and lactate dehydrogenase (LDH). Bile flow and biliary Cd also increased as a result of Picroliv's choleretic property. The Cd-induced serum urea and urinary excretion of proteins, calcium (Ca), Cd and enzymes, such as N-acetyl-beta-D-glucosaminidase (NAG) and LDH, were less marked on Picroliv treatment, indicating recovery from nephrotoxicity. Organ uptake of Cd and essential metals by Cd exposure was reduced on Picroliv treatment. Cd-induced hepatic metallothionein (MT) was lowered by Picroliv, whereas renal MT was unaltered. Cd-induced hepatic damage was also minimized. However, the renal morphological changes were marginally protected by Picroliv. The 12-mg Picroliv dose was more effective than the 6-mg dose in causing amelioration of the above parameters. This study has provided clear evidence for the hepato- and renal protective efficacy of Picroliv against experimental Cd toxicity.
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PMID:Effect of Picroliv on cadmium-induced hepatic and renal damage in the rat. 1716 24

One hundred and ninety-two barrows (Duroc x Landrace x Yorkshire, initial weight 27.7 kg) were used to investigate the effects of cadmium in feed on the function of selected organs and meat colour of growing pigs. The pigs were randomly allocated into four different treatments. Each treatment included three replications with 16 pigs per replicate. The animals were fed corn-soybean basal diet and supplemented with 0, 0.5, 5.0, 10.0 mg/kg cadmium (as CdCl(2)), respectively. The feeding trial ended when the average body weight of the pigs reach 90 kg. The results showed that, compared with controls, addition of 10 mg/kg cadmium to the diet resulted in significant elevations of relative weight of liver and spleen by 18.3% (p<0.05) and 19.7% (p<0.05) respectively, and of serum glutamic-pyruvic transaminase (GPT) and glutamic-oxaloacetic transaminase (GOT) activities by 17.8% (p<0.05) and 27.4% (p<0.05) respectively; and significant decreases of Na(+)/K(+)-ATPase activity in the liver by 24.6% (p<0.05), the redness of longissimus dorsi by 26.6% (p<0.05) and 24.9% (p<0.05) at 0.75 h and 16 h post mortem, respectively, and of the myoglobin content of longissimus dorsi by 19.4% (p<0.05). No changes were found in these indices above when the pigs were fed the diet supplied with 0.5 or 5 mg/kg cadmium (p>0.05), nor in renal functions among cadmium-treatment treatments (p>0.05) as indicated is the activities of urinary N-acetyl-beta-D-glucosaminidase (NAG) and alkaline phosphatase (ALP) and the content of urinary protein. The study indicated the adverse effects of 10 mg/kg cadmium in feed on liver functions and meat colour of growing pigs.
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PMID:Effect of cadmium in feed on organs and meat colour of growing pigs. 1726 Jan 83

Cadmium (Cd(2+)) is a heavy metal that is dispersed throughout the modern environment mainly as a result of pollution from a variety of sources. The aims of the current study were to investigate the efficacy of purified Tunisian montmorillonite clay (TMC) to adsorb Cd, to test the stability of the resulting complex under different conditions in vitro, and to utilize the rat bioassay as an in vivo model to evaluate the protective role of TMC against Cd-induced toxicity and immunodysfunction. In the in vitro study, three concentrations of TMC (0.5, 1.0 and 1.5 g/l aqueous solution) and three concentrations of CdCl(2) (25, 50 and 100 ppm) were tested. The results of the in vitro study showed that TMC had a high capacity of adsorbing Cd at different concentrations tested. The adsorption ranged from 95.7-100% of the available CdCl(2) in aqueous solutions. The complex TMC-Cd was stable at different pHs at 37 degrees C. The in vivo results indicated that treatment with CdCl(2) (2.5 mg/kg BW) for 2 weeks resulted in a significant decrease in triglycerides, total protein, creatinine, creatine kinase, immunoglobulin profile (Ig A and Ig G) and T-cell sub-types (CD3(+), CD4(+), CD8(+) and CD56(+)). Whereas, it significantly increase serum level of AST, ALT, LDH and induced degenerative changes in pro-inflammatory cytokines (TNF-alpha and IL-1). Rats treated with TMC alone (400, 600 and 800 mg/kg BW) were comparable to the control regarding all the tested parameters. The combined treatment of CdCl(2) and TMC at the lowest dose (400 mg/kg BW) showed a significant improvement of all tested parameters. It could be concluded that TMC was effective to protect against Cd hazards at a dose as low as 400 mg/kg BW. These results supported our hypothesis that TMC tightly-bind and immobilized Cd resulted in reduction of metal bioavailability in the gastrointestinal tract.
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PMID:Inactivation of cadmium induced immunotoxicological alterations in rats by Tunisian montmorillonite clay. 1746 9

In an experimental food chain, Wistar rats were fed cadmium (Cd) in an inorganic (CdCl(2)) or organic (mainly associated with metallothionein from Helix aspersa snail viscera) form. After 1 month of exposure to 100 microg inorganic Cd g(-1) in food, an induction of metallothionein was observed in all target tissues. In liver, glutathione peroxidase (GSH-Px) activity decreased and alanine aminotransferase (ALAT) activity increased, suggesting that Cd causes hepatotoxicity. However, lipid peroxidation as well as catalase and caspase 3 (a marker of apoptosis) activities were not modified. At a rather low exposure (2.5 microg Cd g(-1)), metallothionein level in the kidney was found to be the most sensitive biomarker of exposure for both Cd forms. In the small intestine of rats ingesting inorganic Cd, metallothionein expression was significantly higher than that observed for rats fed organic Cd. Present results allowed proposing a simple design to assess the effect of a chemical in a trophic transfer approach.
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PMID:Effects of subchronic digestive exposure to organic or inorganic cadmium on biomarkers in rat tissues. 1753 69

Cadmium fluoride (CdF) is commonly used as an insulator for ulta high speed mass telecommunications equipment, and there is a considerable risk that industrial workers will inhale CdF particles. Despite the possibility that acute exposure can cause harmful systemic effects, there are no studies to date that address the health consequences of acute CdF exposure. This study therefore aimed to determine the acute lethal dose of CdF and its effects on various target organs, including the liver and kidney. We also determined the effect of CdF on serum electrolytes and acid-base balance. The effective lethal dose was determined and dose-response study was conducted after intravenous administration of CdF in rats. The 24 h LD(50) of CdF was determined to be 3.29 mg/kg. The dose-response study used doses of 1.34, 2.67, 4.01 mg/kg CdF. Saline or sodium fluoride solution were used for controles. Severe hepatocellular injury was induced at doses greater than 2.67 mg/kg, as demonstrated by AST and ALT activities greater than 1,500 IU/l in rats injected with a dose of 4.01 mg/kg. Acute renal failure was induced at doses greater than 2.67 mg/kg. Decreased serum Ca, increased serum K and metabolic acidosis were induced at a dose of 4.01 mg/kg. Decreased serum Ca was caused by exposure to ionized F. CdF has the strongest lethal and hepatic toxicity among all Cd containing compounds.
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PMID:Strong acute toxicity, severe hepatic damage, renal injury and abnormal serum electrolytes after intravenous administration of cadmium fluoride in rats. 1757 4

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver.
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PMID:Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats. 1769 48


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