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)

This study was designed to determine the toxic effects of nickel sulfate on the biochemical and elemental profile of liver in protein deficient rats. Nickel sulfate in the dose of 800mg/l in drinking water was administrated to Sprauge Dawley (S.D) normal control as well as protein deficient rats for a total duration of eight weeks. The effects of nickel treatment and protein deficiency when given separately and in combination were studied on rat liver marker enzymes like Alkaline phosphatase (ALP),Glutamate oxaloacetate transaminase (GOT), Glutamate pyruvate transaminase (GPT) and also on the status of essential elements in rat liver. Protein deficient, Ni treated as well as combined protein deficient and nickel treated rats showed significant reductions in the body weight and hepatic protein contents as compared to normal control rats. Hepatic alkaline phosphatase activity and alanine aminotransferase showed a significant elevation in rats subjected to protein deficiency, nickel treatment and combined protein deficiency and nickel treatment. As regards to hepatic levels of aspartate aminotransferase a significant elevation was observed in protein deficient and nickel treated protein deficient animals. Nickel administration to normal and protein deficient rats has resulted in a significant increase in concentrations of nickel, phosphorus and sulfur in liver tissue. The concentration of zinc and copper in liver tissue decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals. Tissue iron concentrations were found to be decreased in protein deficient animals, but the concentrations of iron got elevated significantly in nickel treated and nickel treated protein deficient animals. It has been observed that selenium got decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals when compared to normal animals. The elevation of selenium in nickel treated protein deficient animals was also significantly higher when compared to protein deficient animals.
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PMID:Ineffectiveness of nickel in augmenting the hepatotoxicity in protein deficient rats. 1633 21

We investigated the effect of choice feeding two diets with different selenium (Se) content to young and old moderately Se-deficient laying hens on serum Se (SSe), glutathione peroxidase (GPX), vitamin E, creatine kinase (CK), aspartate aminotransferase (ASAT), thyroxine (T4) and triiodothyronine (T3). Each of two consecutive study parts (I and II) with the same hens and treatments began with a 6-week baseline period (Medium-Se diet), followed by a 9-week depletion period (Low-Se or Medium-Se diet), followed by a 6-week choice period with two different diets offered simultaneously (Medium-Se/Low-Se, Medium-Se/High-Se, or Low-Se/High-Se). During both depletion periods, SSe and GPX gradually decreased, whereas T4 gradually increased in hens fed Low-Se confirming gradual Se-depletion. T3 decreased transiently in young hens only. As reported earlier, Se-deficient hens preferred High-Se over Low-Se diet during the first 3 weeks of choice feeding in part I, not however in part II. This preference resulted in higher SSe in these hens. GPX activity did not reflect feed preference, probably because Se-intake exceeded Se-requirement for maximal GPX activity. In Part II, hens depleted with Low-Se diet had higher SSe when previously offered High-Se diet in either combination, than when offered Low-Se/Medium-Se, presumably due to Se-stores built during choice feeding in part I, which possibly prevented development of Se-deficiency in part II. In addition, in older hens, Se depletion proceeded faster, whereas Se-repletion by choice feeding was slower than in young hens, indicating the increase in Se requirement with advancing age. Vitamin E, ASAT and CK remained largely unchanged by the treatments.
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PMID:Effects of selenium depletion and selenium repletion by choice feeding on selenium status of young and old laying hens. 1637 89

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. The present study was conducted to evaluate the potential toxicity of long time oral exposure to diphenyl diselenide (PhSe)2 in rabbits. Male adult New Zealand rabbits were divided into four groups, group I served as control; groups II, III and IV received 0.3, 3.0 and 30 ppm of (PhSe)2 pulverized in the chow for 8 months. A number of parameters were examined in blood as indicators of toxicity, including delta-aminolevulinate dehydratase (delta-ALA-D), catalase, glutathione peroxidase (GPx), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine, TBARS, non-protein-SH, ascorbic acid and selenium. The results demonstrated that 6 and 8 months of 30 ppm (PhSe)2 intake caused a significant increase in blood delta-ALA-D activity. Erythrocyte non-protein thiol levels were significantly increased after 2 months of 30 ppm (PhSe)2 intake and then return to control levels after prolonged periods of intake. Ingestion of 3.0 ppm of (PhSe)2 for 8 months significantly increased catalase activity in erythrocytes. Conversely, no alterations in GPx, ALT, AST, TBARS and selenium levels were observed in rabbit serum, conversely, selenium levels in peri-renal adipose tissue were significantly increased after 8 months of 30 ppm (PhSe)2 intake, indicating its great lipophylicity. The present results suggest that diphenyl diselenide was not hepato- or renotoxic for rabbits, but caused some biochemical alterations that can be related to some pro-oxidant activity of the compound (particularly the reduction in Vitamin C).
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PMID:Changes in biochemical parameters in rabbits blood after oral exposure to diphenyl diselenide for long periods. 1673 89

Selenoprotein K (SelK) is a newly identified selenoprotein. We showed that selenium incorporation into SelK was dependent on the 3'UTR of SelK mRNA. Sec insertion sequence (SECIS) RNA binding assays demonstrated that human SBP2 bound to the SelK SECIS element through the conserved non-Watson-Crick base pair quartet but not the AAT motif. Examination of the expression pattern revealed that human SelK mRNA was highly expressed in heart. Immunofluorescence analysis showed that SelK localized to the endoplasmic reticulum. Using SelK recombinant adenovirus, we found that overexpression of SelK attenuated the intracellular reactive oxygen species level and protected cells from oxidative stress-induced toxicity in cardiomyocytes. Our findings indicated that SelK is a novel antioxidant in cardiomyocytes and is related to the regulation of cellular redox balance.
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PMID:Identification and characterization of selenoprotein K: an antioxidant in cardiomyocytes. 1696 88

The present study was carried to evaluate the protective effects of melatonin alone and vitamin E with selenium combination against high dose cadmium-induced oxidative stress in rats. The control group received subcutaneous physiological saline. The first study group administered cadmium chloride (CdCl2) by subcutaneous injection of dose of 1 mg/kg. The second study group administered cadmium plus vitamin E with selenium (1 mg/kg sodium selenite with 60 mg/kg vitamin E); the third study group administered cadmium plus 10 mg/kg melatonin (MLT); the fourth study group administered CdCl2 plus a combination of melatonin in addition to vitamin E and selenium for a month. Determination levels of plasma malondialdehyde (MDA), glutathione peroxidase (GSH-Px), blood superoxide dismutase (SOD), creatinine alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen (BUN), and urea were measured in serum. In only CdCl2 administered group, the MDA, creatinine, ALT, AST, ALP, and urea levels in the serum were significantly higher than the control group (p < 0.05). Whereas in all other groups, this values were significantly lower than the only CdCl2 administered group (p < 0.05). Erythrocytes GSH-Px, serum SOD activities of only CdCl2 received group were significantly lower than the control group (p < 0.05). In conclusion, vitamin E + Se, melatonin and vitamin E, and Se, in addition to MLT combinations, had protective effects against high dose cadmium-induced oxidative damage.
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PMID:Effects of selenium and vitamin E, in addition to melatonin, against oxidative stress caused by cadmium in rats. 1787 55

In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.
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PMID:Combined effects of vitamin C, vitamin E, and sodium selenate supplementation on absolute ethanol-induced injury in various organs of rats. 1806 67

1. A trial was conducted to examine the effects of dietary vitamin E content, age and sex on haematological indices and liver enzymes of Japanese quails. A total of 800 1-d-old quail chicks were assigned at random into 4 equal groups and fed on starter and layer diets containing 0, 1, 5 or 10 times the NRC recommended supplements of vitamin E. No selenium was added to the basal deficient diets; the other diets were supplied with 0.2 mg selenium/kg diet. 2. The investigation covered the age span of 3 to 12 weeks in female and male birds. Blood samples were collected at 3-week intervals and tested for haematological indices (erythrocyte count; leucocyte count; susceptibility of erythrocytes to haemolysis; haemoglobin concentration (Hb); packed cell volume (PCV); and mean corpuscular volume (MCV)) and liver enzymes (aspartate transaminase, AST, and glutathione peroxidase, GSH-Px). 3. The significant differences between the 4 dietary treatments indicated that as the levels of selenium and/or vitamin E increased, the percentage of erythrocytes haemolysed and AST activity decreased, whereas Hb and GSH-Px concentrations increased. 4. Differences between age groups showed that older quails had higher erythrocyte susceptibility to haemolysis, higher AST levels and but lower erythrocyte count and PCV. 5. Females had lower erythrocyte haemolysis and higher Hb concentrations than males. 6. The interaction between dietary groups and age groups revealed that the differences between age groups were reduced as the level of selenium and/or vitamin E increased, leading to similar group means over the age period of study. 7. In conclusion, NRC recommended supplements of vitamin E (12 and 25 mg/kg diet) were not adequate. Doses equal to, at least, 5 times that recommended were advised to improve GSH-Px (index of antioxidant status) and Hb concentrations.
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PMID:Effects of vitamin E, age and sex on performance of Japanese quail. 1. Haematological indices and liver function. 1808 49

Twenty male buffalo calves (8-9 months, 112.1 +/- 7.69 kg) were divided into four groups of five animals in each and fed diets without (T1) or supplemented with 0.3 ppm selenium (Se) (T2), 0.3 ppm Se + 10 ppm copper (Cu) (T3), and 10 ppm Cu (T4) for 120 days during which blood samples were collected on day 0, 40, 80, and 120. Concentrations of glucose, total protein, urea, uric acid, and creatinine were similar in all the four groups, but the level of globulin was significantly (P < 0.01) increased in groups T2 and T3, leading to reduced levels of albumin and A:G ratio (P < 0.01) in these groups. The level of different serum enzymes viz. lactate dehydrogenase (LDH), alkaline phosphatase (ALP), glutamate pyruvate transaminase (SGPT), and glutamate oxaloacetate transaminase (SGOT) and hormones viz. T3, T4, testosterone and insulin and T4:T3 ratio were similar (P > 0.05) among the four groups. It was deduced that supplementation of 0.3 ppm Se and/or 10.0 ppm of Cu had no effect on blood metabolic profile in buffalo calves, except for an increased globulin level, indicating improved immunity status of these animals.
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PMID:Effect of selenium and copper supplementation on blood metabolic profile in male buffalo (Bubalus bubalis) calves. 1818 97

Efficacy of thiol chelators viz. N-acetyl cysteine and D-penicillamine (NAC and DPA) along with nutritional supplements viz. zinc acetate, sodium selenite and magnesium sulphate (Zn, Se and Mg) in the treatment of mercury intoxication was investigated in rats. This is of particular interest since high bonding affinity between mercuric ion and the thiol group exits. The mutual antagonism of mercury and selenium is one of the strongest examples of the interaction in the trace element field. Adult rats of Sprague-Dawley strain were administered a bolus dose of dimethyl mercury (10 mg/kg) orally. A significant rise in the aspartate aminotransferase, alanine aminotransferase, serum alkaline phosphatase, lactate dehydrogenase, gamma glutamyltranspeptidase, bilirubin and creatinine were observed. Single mercury exposure also resulted in a significant increase in lipid peroxides with a concomitant decrease in reduced glutathione level in liver, kidney and brain. A decrease in the enzymatic activities of acetyl cholinesterase in different regions of the brain was observed. These parameters were restored considerably with chelating agents along with nutritional supplementation, but NAC+Se and DPA+Mg offered significant protection in comparison with other combinations.
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PMID:Effect of monothiol along with antioxidant against mercury-induced oxidative stress in rat. 1825 9

Two adult and 1 juvenile free-flying greater sandhill cranes (Grus canadensis tabida) were diagnosed with capture myopathy after alpha-chloralose baiting and physical capture during a banding and feeding ecologic study. Blood samples were collected for serum biochemical analysis at the time of capture for the 2 adults, and at 24 hours postcapture, at various intervals during treatment, and at the time of release for all 3 birds. Concentrations of creatine kinase, aspartate transaminase, and lactate dehydrogenase were high within 1 hour of capture and peaked approximately 3 days after capture. By days 10-17 after capture, creatine kinase and lactate dehydrogenase concentrations both decreased to within the reference range measured for cranes at capture, but aspartate transaminase concentrations remained 2-5 times higher than the measured reference range. Treatment consisted of corticosteroids, selenium/vitamin E, parenteral fluids, and gavage feedings. Physical therapy consisted of assisting the cranes to stand and walk 2-8 times a day, massaging leg muscles, and moving limbs manually through the range of motion. The adults were released when they were able to stand up independently and were pacing in the pen. The juvenile was released 12 hours after it was able to stand independently but was returned to the pen when it fell and could not rise. It was treated supportively for an additional 3 days and then successfully released. Both adult cranes were observed on their territories with their original mates after release and returned to their territories for the subsequent 8 years, raising chicks most years. After release, the juvenile was observed in a flock of cranes near its natal territory for the next 2 days.
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PMID:Successful treatment of capture myopathy in three wild greater sandhill cranes (Grus canadensis tabida). 1835 Oct 9


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