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)

Fish serum may reflect status of many biochemical processes in the metabolism. Heavy metals, as environmental stressors, may alter serum biochemical parameters in fishes. Thus, freshwater fish, Oreochromis niloticus, were exposed to low levels (0.05 mg/L) of metals (silver [Ag], cadmium [Cd], copper [Cu], chromium [Cr], zinc [Zn]) to investigate responses of serum biochemical parameters over different exposure periods (0, 5, 10, 20, 30 d). Fish mortality occurred only in Ag exposure, as all fish died between days 12 to 16. Activities of alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) were altered only in Cu- and Cd-exposed fish. Both Cd and Cu exposures decreased the activity of ALP, although they increased the activities of ALT and AST. Glucose concentrations increased in Ag-, Cd-, and Cu-exposed fish, with a sharp increase occurring in Ag-exposed fish before mortality began. Total protein and triglyceride concentrations increased in Ag-exposed fish, although they decreased in Cu-exposed ones. However, all metal exposures increased cholesterol concentration in the serum. Concentration of blood urea nitrogen increased in Ag-, Cd-, and Cu-exposed fish, although it decreased in Cr-exposed ones. Calcium level decreased only in Cu-exposed fish, and Cl(-) level decreased in Ag-exposed fish. Silver and Cu exposures also decreased Na(+) level in the serum. Cadmium and Cu exposures increased serum K(+) levels. The present study, investigating the effects of environmentally realistic metal exposures on serum biochemical parameters, demonstrated that fish serum could sensitively reflect environmental metal stress. Thus, it suggests that serum biochemical parameters could be used as important and sensitive biomarkers in ecotoxicological studies concerning the effects of metal contamination and fish health.
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PMID:Changes in serum biochemical parameters of freshwater fish Oreochromis niloticus following prolonged metal (Ag, Cd, Cr, Cu, Zn) exposures. 1834 36

The purpose of this study was to examine concentrations of selected heavy metals in the liver and kidney of brown hares (Lepus europaeus). In addition, correlations between heavy metals and biochemical parameters in blood plasma were determined. The average concentrations of heavy metals (mmol/L) +/- SD were as follows: liver: Pb 0.221 +/- 0.189, Cd 0.160 +/- 0.140, Hg 0.021 +/- 0.030, kidney: Pb 0.115 +/- 0.125, Cd 1.570 +/- 1.103, Hg 0.030 +/- 0.053. The average concentrations of biochemical parameters in the blood plasma were as follows: Ca 3.16 mmol/L, P 2.19 mmol/L, Mg 1.40 mmol/L, Na 148.71 mmol/L, K 8.12 mmol/L, glucose 6.56 mmol/L, total proteins 56.49 g/L, urea 5.00 mmol/L, total lipids 1.40 g/L, bilirubin 3.97 micro mol/L, cholesterol 1.53 mmol/L, aspartate aminotransferase (AST) 6.06 micro kat/L and alanine aminotransferase (ALT) 1.94 micro kat/L. Average levels of hormones (ng/mL) were as follows: testosterone 2.94, androstendiol 0.13, estradiol 501.59, progesterone 6.63, oxytocin 328.60. Tissue analysis showed an accumulation of lead, cadmium and mercury in the liver and kidney of brown hares. There were no significant correlations between levels of heavy metals in liver, kidney, and biochemical parameters.
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PMID:Environmental levels of cadmium, lead and mercury in brown hares and their relation to blood metabolic parameters. 1839 73

Licorice is commonly used as a cure for digestive disorders and as a detoxification agent in East Asia. This study investigated the protective effect of licorice water extract against cadmium (CdCl(2), Cd)-induced liver toxicity in rats. To induce acute toxicity, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously (i.v.) injected into rats. The rats then received either a vehicle or licorice water extract (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd 24 h after the last licorice/vehicle treatment. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with licorice reduced ALT, AST and LDH. In histopathological analysis, licorice decreased the central necrosis around central veins, the peripheral hemorrhage around portal triads, the percentage of degenerative hepatic regions (%/mm(2) hepatic parenchyma) and the number of degenerative hepatic cells (N/100 hepatic cells). Licorice also inhibited the increment of Bad (a BH3 domain-containing protein) translocation by Cd in liver cells. These results demonstrate that licorice could have a hepatoprotective effect by inhibiting the translocation of Bad to the mitochondria in Cd-intoxificated rats.
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PMID:Hepatoprotective Activity of Licorice Water Extract against Cadmium-induced Toxicity in Rats. 1895 29

The hepatoprotective effect of onion and garlic extracts on cadmium (Cd)-induced oxidative damage in rats is reported. Control group received double-distilled water alone. Cd group was challenged with 3CdSO(4).8H(2)O (as Cd; 1.5 mg/kg bw per day per oral) alone, while extract-treated groups were pretreated with varied doses of onion and/or garlic extract (0.5 and 1.0 ml/100 g bw per day per oral) for a week and thereafter co-treated with Cd (1.5 mg/kg bw per day per oral) for 3 weeks. Cd caused a marked (p < 0.001) increase in the levels of lipid peroxidation and glutathione S-transferase, whereas glutathione, superoxide dismutase, and catalase levels were decreased in the liver. We also observed a decrease in hepatic activities of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase and a concomitant increase in the plasma activities of ALT and AST. Onion and garlic extracts significantly attenuated these adverse effects of Cd. Onion extract proffered a dose-dependent hepatoprotection. Our study showed that Cd-induced oxidative damage in rat liver is amenable to attenuation by high dose of onion and moderate dose of garlic extracts possibly via reduced lipid peroxidation and enhanced antioxidant defense system that is insufficient to prevent and protect Cd-induced hepatotoxicity.
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PMID:Hepatoprotective potentials of onion and garlic extracts on cadmium-induced oxidative damage in rats. 1908 32

The research was conducted to investigate the toxic effects of cadmium chloride (CdCl2), administered during gestation period on female Wistar rats. Pregnant rats received CdCl2 (20 mg/l, orally) from Day 6 to Day 19 of pregnancy. Results showed that Cd treatment induced a decrease in body weight gain. The relative liver weight increased significantly, with a marked decrease of glycogen and total lipids content. The administration of Cd induced hepatotoxicity as indicated by elevations in plasma alanine aminotransferase (ALT), aspartate aminotransferase and lactate dehydrogenase (LDH) activities (p < 0.05). Treatment with CdCl2 caused a significant (p < 0.05) increase in glucose. A significant increase was observed in the level of MDA and 8-oxodGuo tissues in the cadmium-exposed group compared to the control group (p < 0.05). Results showed that cadmium given to dams led to an oxidative stress and DNA damage in tissues of pregnant rats.
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PMID:Changes in antioxidant status and biochemical parameters after orally cadmium administration in females rats. 1937 26

This experiment pertains to the protective role of naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5mg/kg) was administered orally for 4 weeks to induce hepatotoxicity. Liver damage induced by cadmium was clearly shown by the increased activities of serum hepatic marker enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and serum total bilirubin (TB) along with the increased level of lipid peroxidation indices (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) and protein carbonyl contents in liver. The toxic effect of cadmium was also indicated by significantly decreased levels of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C and vitamin E). Administration of naringenin at a dose of (50mg/kg) significantly reversed the activities of serum hepatic marker enzymes to their near-normal levels when compared to Cd-treated rats. In addition, naringenin significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. The histopathological studies in the liver of rats also showed that naringenin (50mg/kg) markedly reduced the toxicity of cadmium and preserved the normal histological architecture of the tissue. The present study suggested that naringenin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of rats.
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PMID:Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin. 1940 69

The present study was designed to evaluate the protective effect of some local medicinal plants against liver and kidney toxicity induced by cadmium chloride. Methanolic extracts of Acacia nilotica and Retama raetam were used in this study. Furthermore, histopathological and histochemical investigations were done. Cadmium chloride caused a significant increase in serum AST, ALT, ALP, bilirubin, urea, and creatinine, cholesterol, LDL, triglycerides, and HDL levels Administration of Acacia nilotica and Retama raetma significantly inhibit that increase. Cadmium chloride induced a significant decrease in serum total protein, albumin, globulin levels, albumin/globulin ratio, blood SOD, and GPx, while Acacia nilotica and Retama raetam increase. Cadmium chloride caused a significant increase in MDA and NO, while a significant decrease in MDA and NO after Acacia nilotica and Retama raetam administration. These results suggested a beneficial effect of these plant extracts against experimentally-induced hepato- and nephro-toxicity of cadmium, and the possible mechanism of the protective effects may be partly due to the antioxidant activity of these plants.
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PMID:Role of some Egyptian medicinal plants against liver and kidney toxicity induced by cadmium chloride. 1981 61

This study sets out to compare the absorption and toxicity of Cadmium (Cd) administered via the food-chain and inorganic Cd administered in drinking water after 1 and 3 months exposure using rats as animal model. The food-chain was mimicked by exposing rats to diet containing Cd pre-exposed fish. The uptake of Cd by the rats after both mode of exposure was calculated by summing up the Cd burden in the liver and kidneys and was expressed in terms of % intake. The toxicity of Cd was assessed by monitoring biochemical indices of liver function in the plasma and liver. Regardless of the mode of exposure of the rats, the Cd load in the liver and kidney was significantly (P < 0.05) higher than the respective controls with the kidney having a significantly higher load than the liver after both periods of exposure. However irrespective of the mode of exposure, more Cd was accumulated in the liver and kidney of the 3 months exposed rats relative to those exposed for 1 month. The uptake of Cd by rats exposed to Cd via the food-chain for 1 and 3 months was significantly (P < 0.05) lower when compared to the corresponding water mediated Cd exposed rats, except for the liver after 3 months of exposure. The liver L-ALT activity of rats administered inorganic Cd in drinking water for 1 and 3 months was significantly (P < 0.05) lower as compared to controls. Parallel analysis of the plasma showed no significant (P > 0.05) difference in L-ALT activity between both groups after the same periods of exposure. The L-AST activity in the plasma of rats similarly exposed to Cd for 1 and 3 months was significantly (P < 0.05) higher as compared to controls with a corresponding reduction in the liver. Conversely no significant (P > 0.05) change was observed in plasma and liver L-ALT and L-AST activities after food-chain mediated exposure to Cd for 1 and 3 months in relation to their respective controls. These findings indicate that Cd incorporated in fish is more easily bioavailable, but less toxic relative to inorganic Cd salts at the end of 3 months of exposure in rats.
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PMID:Comparative effect of water and food-chain mediated cadmium exposure in rats. 2019 6

Cadmium (Cd) is a non-essential element and is a widespread environmental pollutant. Exposure to cadmium can result in cytotoxic, carcinogenic and mutagenic effects. The aim of the current work was to evaluate the protective effect of Aquilegia vulgaris extract against the oxidative stress and the genotoxicity induced by Cd using the chromosomal aberrations in somatic and germ cells assay and random amplified polymorphism DNA (RAPD-PCR) analysis. Forty male Balb/c mice were divided into four groups including the control group, Cd-treated group and the groups treated with the extract alone or plus Cd. The results indicated that Cd increased serum ALT, AST, urea, LDH, CK, lipid peroxidation in liver tissue accompanied with a significant decrease in GPX and SOD. Cd also increased the number of chromosomal aberrations in bone marrow and spermatocytes including structural and numerical aberrations. Animals treated with the extract alone were comparable to the control regarding all the tested parameters. The extract succeeded in preventing or diminishing the oxidative stress and the clastogenic effects of Cd. It could be concluded that Aquilegia vulgaris extract is a promising protective agent against oxidative stress and genotoxicity during the exposure to Cd.
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PMID:Aquilegia vulgaris extract protects against the oxidative stress and the mutagenic effects of cadmium in Balb/c mice. 2020 84

We examined the sensitivity of metallothionein (MT)-III null mice to cadmium (Cd)-induced acute hepatotoxicity. MT-I/II null mice were also used to compare Cd toxicities between MT-III null mice and MT-I/II null mice. Male MT-I/II null mice, MT-III null mice and wild-type mice were given s.c. injection of Cd (5-20 micromol/kg) and then the blood and liver were collected from each mouse under ether anesthesia at 2 days after the administration. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities elevated by injection of Cd were significantly higher in the MT-I/II null mice than in the wild-type mice. In the MT-III null mice, ALT and AST activities were not elevated following the injection of Cd. Further, marked morphological changes such as necrosis of hepatocytes, severe hemorrhage and congestion were observed by injection of Cd in both MT-I/II null mice and wild-type mice, whereas the degree of injury was found to be more extensive in MT-I/II null mice. In contrast, only occasional damage was observed in the liver of MT-III null mice treated with the same dose of Cd. These morphological observations were consistent with the results of ALT and AST activities. In the present study, it was clearly found that MT-III null mice were resistant to Cd hepatotoxicity, although MT-I/II null mice were sensitive to its toxicity. MT-III may be an accelerative factor in Cd-induced acute hepatotoxicity.
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PMID:Resistance of metallothionein-III null mice to cadmium-induced acute hepatotoxicity. 2037 71


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