Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult male rats were injected sc with cadmium chloride (CdCl(2)) in a single dose of 7 mg/kg body wt. Twenty-four hours postinjection, exposure to CdCl(2) increased the hemoglobin absorbance of the testes from 0.36 +/- 0.01 to 2.46 +/- 0.02. Pretreatment of rats with chlorpromazine (CPZ) 3 mg/kg ip either for 1 or 2 days before exposure to CdCl(2) significantly (p < 0.05) reduced the testicular damage and the hemoglobin absorbance decreased to 1.03 +/- 0.02 and 0.92 +/- 0.04, respectively. After CdCl(2) injection there was a progressive increase in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. CdCl(2) injection induced hemorrhage and a diffuse area of coagulative necrosis in liver. Pretreatment with CPZ partially protected liver from the effect of CdCl(2). Two months postinjection, exposure to CdCl(2) significantly decreased the weights of testes, epididymis, and accessory sex organs. Furthermore, CdCl(2) induced a highly significant (p < 0.01) decrease in sperm cell concentration and the percentage of mobile cells. Moreover CdCl(2) induced degenerative changes in testes, epididymis, and seminal vesicles. Pretreatment with CPZ partially protected these organs from the toxic effects of CdCl(2). It could be concluded that chlorpromazine partially antagonized the toxic effects of cadmium on liver, testes, and other male reproductive organs of rats.
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PMID:The antagonistic effect of chlorpromazine on cadmium toxicity. 1055 21

Stress responses and changes in protein metabolism were studied in common carp Cyprinus carpio exposed to 0, 0.8, 4, and 20 microM cadmium (Cd) over a 29-day period. Blood and other tissue samples were taken after 4 and 29 days of exposure. The highest Cd concentration proved to be lethal to the fish, resulting in 100% mortality after 21 days of exposure. Cd accumulated in the tissues in the following order: kidney>liver>gills. Blood hematocrit, blood hemoglobin, plasma glucose, plasma lactate, and tissue total protein contents were not significantly altered. The concentrations of Cd and zinc (Zn) binding metallothioneins ((Cd, Zn)-MTs) were in the following order=liver>kidney>gills. An increase in (Cd, Zn)-MTs was observed at all exposure concentrations at days 4 and 29 in kidney and at Day 29 in gills. No significant changes in (Cd, Zn)-MT contents were found in liver. The concentrations of free amino acids and the activities of proteases were increased at Day 4 in gills, liver, and kidney of carp exposed to 4 and 20 microM Cd, and in gills and kidney at Day 29 in carp exposed to 4 microM Cd. The observed increases in the activities of aspartate aminotransferase and alanine aminotransferase suggest that the observed proteolysis is intended to increase the role of proteins in the energy production during Cd stress. However, this increased activity of both aminotransferases was not found in gills during exposure to the lethal Cd concentration, indicating that Cd may also cause an inhibitory effect on the activity of these enzymes above a certain level.
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PMID:Stress responses and changes in protein metabolism in carp Cyprinus carpio during cadmium exposure. 1122 34

In vitro study for the determination of the toxicity of some pesticides (glyphospate and paraquat) and cadmium chloride (CdCl2) on the activities of serum acetylcholinesterase (AChE), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), and acid phosphatase (AcP) is described. Changes in electrophoretic patterns of serum proteins were also tested. Results revealed that glyphosate was effective on all enzymes except AcP. Its IC50 values (the concentration of compound that inhibits 50% of the enzyme activity in 1 h at 37 degrees C) were 714.3, 750, 54.2, 270.8, and 71.4 mM for AChE, LDH, AST, ALT, and AlP, respectively. The inhibitory effect of paraquat varied markedly among all enzymes. The IC50 values of paraquat were 321.4 and 750 mM for AST and ALT, respectively. It had mild effect on AChE and LDH; and no effect on the activities of AlP and AcP. The effect of CdCl2 was pronounced with AChE, ALT, AlP, and AcP, and no effect on LDH and AST was found. The corresponding IC50 values were 77.7, 22.2, 33.3, and 83.3 mM for AChE, ALT, AlP, and AcP, respectively. Polyacrylamide gel electrophoretic patterns of serum proteins showed marked differences with glyphosate and CdCl2 but not with paraquat. The results suggest that the in vitro enzyme-activity test seems to have a potential for the assessment of pesticide and heavy metal toxicity.
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PMID:Influence of paraquat, glyphosate, and cadmium on the activity of some serum enzymes and protein electrophoretic behavior (in vitro). 1128 Dec 53

A study was undertaken to investigate the effect of taurine on the toxicity of cadmium in male Wistar rats. The rats were divided into six groups and fed different diets with or without supplement of 5% taurine and 150-300 ppm cadmium for 2 months. It was found that the body weight of rats, the ratios of liver and kidney weight to body weight, and the level of glutathione in the liver were decreased with increasing the dose of cadmium. The levels of cadmium in the liver and kidney, the levels of thiobarbituric acid-relative substances (TBARS) in the plasma and liver, the activities of aspartate transaminase (AST) and alanine transaminase (ALT) in the plasma, and the levels of blood urea nitrogen (BUN) and creatinine in the plasma of rats were increased with the increasing dose of cadmium. Hence, symptoms of cadmium toxicity in rats included loss of body weight, hepatotoxicity and nephrotoxicity. However, these toxic effects of cadmium were significantly reduced when the rats fed diet with supplement of taurine. Furthermore, the level of cadmium in the feces of rats treated with taurine and cadmium was higher than that of rats treated with cadmium alone. It indicated that taurine might play a role in reducing the toxic effect of cadmium in rats.
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PMID:Effect of taurine on toxicity of cadmium in rats. 1157 96

To clarify the action of estrogenic endocrine disruptors on cadmium (Cd)-induced metallothionein (MT) synthesis in the liver, we investigated the effects of bisphenol A (BPA) on hepatic MT-I mRNA expression and MT contents after Cd injection. Liver damage after Cd injection was assessed by measuring glutamic-pyruvic transaminase (GPT) and glutamic-oxaloacetic transaminase (GOT) activities in the serum. It was found that BPA reduced the Cd-induced expression of MT-I mRNA and MT protein in the liver. The administration of tamoxifen, an estrogen receptor antagonist, prevented the reduction of hepatic MT content by PA. Moreover both the GPT and GOT activities of the BPA-treated groups were higher than those of the control groups. These findings suggest that BPA reduced hepatic MT synthesis after Cd injection via the estrogen receptor which resulted in increased damage to the liver.
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PMID:Bisphenol A enhances cadmium toxicity through estrogen receptor. 1177 54

Several compounds have been shown to cause acute toxicity to cadmium (Cd). The mechanism of tolerance to Cd toxicity induced by glucocorticoids or by inflammation involves induction of metallothionein (MT) synthesis via glucocorticoid response elements or by inflammatory cytokines. We have demonstrated previously that the synthetic glucocorticoid dexamethasone suppresses inflammation-mediated induction of hepatic MT synthesis. Here we investigated the effect of glucocorticoid on tolerance to Cd induced by inflammation in mice. The LD50 of Cd for mice with induced inflammation by injection with turpentine oil (Tur-mice) was higher than the LD50 in control mice. Pretreatment of Tur-mice with dexamethasone to the Tur-mice (Dex+Tur-mice) resulted in a decrease in LD50 after Cd treatment. A significant increase in plasma alanine aminotransferase and aspartate aminotransferase levels in the Dex+Tur-mice was observed at lower doses of Cd than in the Tur-mice and at higher doses of Cd than in control mice. Dexamethasone did not suppress tolerance to cadmium toxicity in the testes of the Tur-mice. Pretreatment of Tur-mice with dexamethasone resulted in suppression of both plasma interleukin (IL)-6 elevation and in suppression of hepatic MT levels when induced by inflammation but not when induced by Cd. These data suggest that suppression of tolerance to Cd toxicity induced by glucocorticoid may involve hepatic MT synthesis mediated by inflammatory cytokines, such as IL-6. We suggest that the inflammatory response can modulate Cd toxicity by induction of MT by inflammatory cytokines.
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PMID:Glucocorticoids suppress the inflammation-mediated tolerance to acute toxicity of cadmium in mice. 1178 Oct 73

The efficacy of Emblica officinalis in modifying the acute cytotoxicity of cadmium in male rats was evaluated. Oral administration of Emblica fruit juice (500 mg/kg, b.w.) for 8 days followed by a single toxic dose of Cd as CdCl2 (3 mg/kg,b.w. ip), considerably reduced the mortality in rats as well as prevented to some extent the cadmium induced histopathological damage in testis, liver and kidneys. Biochemical investigation also revealed reduced levels of Cd induced serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and gamma glutamyltranspeptidase. The enhanced levels of Cd and lipid peroxidation in liver, kidney, and testes and metallothionein and total sulphydryl in liver and kidney by Cd were significantly reduced by Emblica pretreatment. These results suggest cytoprotective potential of Emblica fruit in acute cadmium toxicity which could be due to its multiple role in biological system.
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PMID:Modulation of acute cadmium toxicity by Emblica officinalis fruit in rat. 1262 3

Cadmium is a dangerous occupational and environmental toxin. It accumulates in the human organism mainly in liver and kidneys. Cadmium half-life is about 10 years, so the symptoms of cadmium intoxication may occur several years after the exposure. Until now in treating intoxication with this metal chelating compounds have been used, burdened with numerous undesirable symptoms. In our investigations anthocyanins from Aronia melanocarpa were used to reduce the harmful results caused by cadmium. Administering anthocyanins with cadmium chloride resulted in a statistically significant decrease of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity, concentration of bilirubin and urea in blood serum and decreased cadmium cumulation in liver and kidneys in relation to animals receiving cadmium chloride only.
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PMID:Effect of anthocyanins on selected biochemical parameters in rats exposed to cadmium. 1283 79

Cadmium is a well-known human carcinogen and a potent nephrotoxin. Lipid peroxidation is involved in cadmium-related toxicity. Vitamin E and beta-carotene are effective antioxidants and free radical scavengers. Therefore, the present study was carried out to investigate the potential protective effects of vitamin E and beta-carotene alone or in combination against cadmium (Cd) toxicity. Cadmium chloride (CdCl2, 5 mg/kg BW, 1/15 LD50), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E with beta-carotene (100 + 10 mg/kg BW, respectively) were orally administered by gavage alone or in combination. The tested doses were given to rats every other day (15 times). Results obtained showed that CdCl2 significantly (P < 0.05) induced free radicals in plasma, liver and brain. The activities of glutathione S-transferase (GST) (plasma and liver), alkaline phosphatase (AlP) (plasma and liver), aspartate aminotransferase (AST), alanine aminotransferase (ALT) (liver) and acetylcholinesterase (AChE) (plasma and brain) were significantly (P < 0.05) decreased due to CdCl2 administration, whereas, the activities of AST and ALT were increased in plasma. Treatment with CdCl2 caused a significant (P < 0.05) increase in glucose, urea, creatinine and bilirubin in plasma. On the other hand, results showed that CdCl2 significantly (P < 0.05) decreased plasma total protein (TP), albumin (A), blood hemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), while total leukocyte count (TLC) increased. Treatment with CdCl2 caused a significant (P < 0.05) decrease in sperm concentration, motility (%), weight of testes and epididymis, and increase in dead and abnormal sperm. Results demonstrated the beneficial influences of vitamin E, -carotene alone and/or in combination in reducing the harmful effects of CdCl2.
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PMID:Cadmium-induced changes in lipid peroxidation, blood hematology, biochemical parameters and semen quality of male rats: protective role of vitamin E and beta-carotene. 1530 3

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. In the present investigation subchronic deleterious effects of cadmium-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 (5 micromol/kg) were studied. Male adult Swiss albino mice (25-35 g) received CdCl2 (10 micromol/kg, subcutaneously), five times/week, for 4 weeks. A number of toxicological parameters in blood, liver, kidney, spleen and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation and ascorbic acid content, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine and lactate dehydrogenase (LDH) were also determined. The results demonstrated that cadmium caused inhibition of delta-ALA-D activity in liver (24%), kidney (33%) and spleen (73%) and (PhSe)2 therapy was effective in restoring enzyme activity in all tissues. A reduction in ascorbic acid content was observed in kidney (11%) and spleen (10.7%) of cadmium-treated mice and (PhSe)2 was only effective in improving this reduction in kidney. An increase of lipid peroxidation induced by cadmium was noted in liver (29%) and brain (28%) tissues and (PhSe)2 therapy was effective in restoring TBARS levels in both tissues. We also observed an increase on plasma LDH (1.99-times), AST (1.93-times) and ALT (4.24-times) activities. (PhSe)2 therapy was effective in restoring AST activity at control level. (PhSe)2 did not present toxic effects when plasma parameters were evaluated. The results suggest that the administration of an antioxidant (PhSe)2, during cadmium intoxication may provide beneficial effects by reducing oxidative stress in tissues.
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PMID:Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues. 1573 37


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