UNIPROT:P17174 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatoprotective activity of the aqueous-methanolic extract of Ambrosia maritima was investigated against acetaminophen (paracetamol, 4-hydroxy acetanilide) induced hepatic damage. Acetaminophen at the dose of 640 mg/kg produced liver damage in rats as manifested by the significant (P < 0.001) rise in serum levels of glutamate oxaloacetate transaminase (AST), glutamate pyruvate transaminase (ALT) and alkaline phosphatase (ALP) to 1178.5 +/-118.05; 607.5 +/- 32.6 and 274.16 +/- 8.89 IU/l (n = 10), respectively, compared with respective control values of 97.83+/-3.23; 46.0 +/- 3.92 and 168.67 +/- 7.86 IU/l. Pretreatment of rats with the plant extract (100 and 200 mg/kg) lowered significantly (P < 0.001) the respective serum AST to 203.3+/-5.74 and 157.1 +/- 8.78 IU/l, ALT to 138.67 +/- 7.7 and 87.5 +/- 3.6 IU/l and ALP levels to 238.0 +/- 5.89 and 206.5 +/- 7.5 IU/l, respectively. Treatment of rats with acetaminophen led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA) (42%). This was associated with a significant reduction of the hepatic antioxidant system e.g. reduced glutathione (GSH) (65%), glutathione reductase (GSH-R) (35%), total glutathione peroxidase (GSH-Px) (32%) and glutathione-S-transferase (GST) (16%). These biochemical alterations resulting from acetaminophen administration were inhibited by pretreatment with A. maritima L. extract. These data suggest that the plant A. maritima L. may act as a hepatoprotective and antioxidant agent.
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PMID:Evaluation of the protective potential of Ambrosia maritima extract on acetaminophen-induced liver damage. 1129 46

The aims of the present study were first to compare the effects of melatonin and vitamin E on the cholestasis syndrome and their protective effect on liver injury, and second, to evaluate the activity of antioxidant enzymes after treatment with these antioxidant drugs. Cholestasis was achieved in adult male Wistar rats by double ligature and section of the extra-hepatic biliary duct. Hepatic and plasma oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA) and reduced glutathione (GSH) in plasma and homogenates of hepatic tissue. Serum bilirubin, alkaline phosphatase (AP), and gamma-glutamyl-transpeptidase (GGT) were used to evaluate the severity of cholestasis, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were used to evaluate the hepatic injury. Both vitamin E and melatonin were administrated 1 day before and 7 days after bile duct ligation. Acute ligation of the bile duct was accompanied by a significant increased in MDA and a decrease in GSH levels in both plasma and liver, as well as a significant reduction in antioxidant enzymes activities. The overall analysis of both treatments showed that melatonin (500 microg/kg daily) offered significantly better protection against cholestasis and a superior protective effect on hepatic injury than did vitamin E (15 mg/kg daily). Although vitamin E treatment resulted in a reduction of parameters of oxidative stress, the results were significantly better after a much lower daily dose of melatonin. Moreover, melatonin treatment was associated with a significant recovery of antioxidative enzymes. In conclusion, the present paper demonstrates a correlation between the intensity of biliary tract obstruction and increased free radical generation, as well as a direct correlation between the level of oxidative stress and the biochemical markers of liver injury. Melatonin (at a much lower dose than vitamin E) was much more efficient than vitamin E in reducing the negative parameters of cholestasis, the degree of oxidative stress and provided a significantly greater hepatoprotective effect against the liver injury secondary to the acute ligation of the biliary duct.
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PMID:Melatonin versus vitamin E as protective treatment against oxidative stress after extra-hepatic bile duct ligation in rats. 1155 69

Cocaine remains a widely abused substance. While most addicts take cocaine intranasally, a considerable number abuse cocaine by mouth. It has been assumed that after oral exposure cocaine is hydrolyzed in the stomach rendering it ineffective. This study investigated the effect of orally administered cocaine on liver function and integrity as well as its effect on liver and blood antioxidative enzymes. Male CF-1 mice were orally administered either 0, 5, 10 or 20 mg cocaine/kg body weight and sacrificed 24 h after the last treatment. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured as markers of liver injury. Blood and liver glutathione (GSH) levels were determined as well as the activities of glutathione peroxidase (GPx) and catalase (CAT). In addition, the activity of liver glutathione reductase (GRx) was also measured. The results demonstrated that oral cocaine caused hepatotoxicity in a dose dependent manner. Serum ALT and AST were elevated while blood GSH concentration decreased in all cocaine treated animals. In addition, there was a significant dose dependent decrease in the activities of GPx and CAT in blood and liver of cocaine treated animals. However, hepatic GSH content and GRx activity manifested a significant increase, particularly in the group, which received 20 mg/kg cocaine. This study is the first to demonstrate that cocaine-induced hepatotoxicity results following the oral route of administration.
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PMID:Oral cocaine produces dose-related hepatotoxicity in male mice. 1170 Dec 20

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation or cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (CSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters-GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.
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PMID:Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats. 1173

This work examines the effects of lyophilized extracts of the medicinal plants Rhazya stricta, Balanites aegyptiaca and Haplophylum tuberculatum on liver damage induced by paracetamol in mice. Rapid HPLC finger prints for some of these extracts were made. The hepatoprotective effects of the plant extracts were compared with that of the standard hepatoprotective agent silymarin. The extracts (1 g/kg) and silymarin (0.1 g/kg) were given orally for 5 consecutive days. On the last day of treatment a hepatotoxic oral dose of paracetamol (0.6 g/kg) was given, and 3 h later, the hepatic function of mice was evaluated using pentobarbitone -induced sleeping time, the concentration of reduced glutathione (GSH) in liver, and the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT) and cholesterol concentration in plasma. The livers were weighed and examined for macro- and microscopic changes. Pretreatment with R. stricta or with silymarin protected the livers of treated mice against paracetamol hepatotoxicity as evidenced by a significant improvement of the above liver function tests. B. Aegyptiaca had a relatively modest hepatoprotective activity, while H. tuberculatum was almost ineffective. Oral pretreatment of mice for 5 consecutive days with an extract of R. stricta or silymarin protected about 57% and 92% of the treated mice, respectively, against the lethal effect of paracetamol (1 g/kg). B. aegyptiaca and H. tuberculatum protected only 27% and 16% of the animals, respectively.
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PMID:Effect of the traditional medicinal plants Rhazya stricta, Balanitis aegyptiaca and Haplophylum tuberculatum on paracetamol-induced hepatotoxicity in mice. 1174 41

During water treatment, potentially hazardous chemical by-products may be formed. Alachlor (2-chloro-N-(2, 6-diethylphenyl)-N-(methoxymethyl) acetamide) is a widely used pre-emergence herbicide. The present study investigated the toxicity of alachlor and its disinfection by-products on freshly isolated rat hepatocytes. Hepatocytes were harvested by a collagenase perfusion technique and were exposed to different concentrations of alachlor and its by-products for up to 2 h. Cell viability, the leakage of aspartate transaminase (AST) and alanine transaminase (ALT) and glutathione (GSH) depletion were determined throughout the incubation period. The cell viability of the hepatocytes exposed to 100 microg ml(-1) alachlor was decreased by 20% compared with the control after 60 min of incubation. At the same concentration of alachlor the leakage of ALT and AST was increased by 56% and 45%, respectively. Cell viability of the hepatocytes was decreased upon exposure to 2-chloro-N-(3-chloro-2,6-diethylphenyl)-N-(methoxymethyl) acetamide (CCDMA) and 2-chloro-N-(3-chloro-2,6-diethylphenyl) acetamide (CCDA)--the by-products of alachlor and chlorine--after 60 min of exposure. At 100 microg ml(-1) CCDMA the AST leakage was increased significantly (73%) after 30 min of incubation. The reaction mixture of alachlor (100 microg ml(-1)) and chlorine dioxide (1 ppm) caused significant increases in cell loss and ALT and AST levels by 22%, 40% and 34%, respectively, as early as 15 min incubation. Alachlor (100 and 200 microg ml(-1)) caused significant decreases in GSH contents (62%) in isolated hepatocytes. The reaction mixture of alachlor and chlorine dioxide led to significant glutathione depletion (44%) after 60 min of incubation. The by-products of alachlor and chlorine--CCDMA and CCDA--depleted GSH almost completely (93%). This investigation suggested that the by-products formed from the reaction of alachlor and chlorine decreased GSH and increased the leakage of liver enzymes, especially AST.
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PMID:In vitro hepatotoxicity of alachlor and its by-products. 1180 27

Prolonged low-medium intensity exercise is associated with increased oxidative stress in humans. We hypothesized that competitive equine endurance racing would induce changes in circulatory antioxidants and produce systemic oxidative stress. Forty horses competing in a 140-km endurance race in warm conditions [shade temperature 15-19 degrees C; 62-88% relative humidity (%RH)] were sampled before (Pre), immediately after exercise (End) and at approximately 16 h into recovery (+16 h). Plasma ascorbic acid concentration was not different between Pre [11.1 (median); 4.6-20.3 micromol/L (range)] and End [9.7; 3.0-38.9 (range) micromol/L] but was significantly decreased at +16 h (5.5; 2.8-15.5 micromol/L; P < 0.05). Total red cell hemolysate glutathione (TGSH) concentration was significantly reduced by exercise (Pre 1261; 883-1532 micromol/L; End 1065; 757-1334 micromol/L; P < 0.05) and at +16 h recovery (1032; 752-1362 micromol/L; P < 0.05). Glutathione redox ratio was unchanged by exercise but was significantly decreased at +16 h compared with that at both Pre and End (P < 0.05). The concentration of total barbituric acid reactive substances (TBARS) in plasma was increased compared with that at Pre (309; 66-1048 nmol/L), both at End (408; 170-1196 nmol/L; P < 0.05) and +16 h (380; 99-1161 nmol/L; P < 0.05). alpha-Tocopherol was unchanged by exercise or recovery. Mean race speed was 16.5 +/- 1.6 km/h and ranged from 13.9 to 19.7 km/h. Mean speed during competition in horses that completed the full 140 km (n = 28) was significantly correlated with end of exercise ascorbic acid (r = 0.622; P = 0.0004). Although there were increases in creatine phosphokinase (CK), aspartate aminotransferase (AST) and TBARS and a loss of TGSH, this study failed to demonstrate evidence of classical oxidative stress.
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PMID:Changes in circulatory antioxidant status in horses during prolonged exercise. 1204 74

Tobacco smoke is involved in the pathogenesis of several diseases regarding different body systems, mainly cardiovascular and respiratory in addition to its local toxic effect in the oral cavity. The noxious effects of smoke compounds justify the high incidence of periodontal diseases, caries, and neoplastic diseases of oral tissues in smokers. Some toxic components of tobacco smoke, unsaturated and saturated aldehydes, could interact with thiol rich compounds, leading to structural and functional modification of these molecules. Previous papers have demonstrated an in vitro significant decrease of some enzymatic activities, both in plasma and in saliva, following external addition of aldehydes or exposure to cigarette smoke (CS). Furthermore, the same studies underlined the protective effect exerted by the addition of glutathione (GSH) against the damaging role of smoke aldehydes. In this study some salivary enzymes (lactic dehydrogenase [LDH], aspartate aminotransferase [AST] and amylase), and total GSH were measured in 20 volunteers smokers, before and just after smoking a single cigarette. All enzymatic activities showed a significant inhibition following a single cigarette, probably due to the interaction between smoke aldehydes and -SH groups of the enzyme molecules. Moreover, the percentage of the enzymatic inhibition showed a negative correlation with the basal level of salivary GSH. Our results emphasize that not only one cigarette is sufficient to impair the salivary enzymatic activities but also strengthen the proposed protective role of GSH against the noxious biochemical effects of CS.
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PMID:Inhibition of salivary enzymes by cigarette smoke and the protective role of glutathione. 1204 26

The present investigation focused on the possible hepatoprotective potential of captopril on carbon tetrachloride (CCl4)-induced acute liver injury in mice. Twenty-four hours after a single intraperitoneal injection of CCl4 (20 microl/Kg), hepatotoxicity was evidenced in the serum by elevated levels of aspartate transaminase (AST; EC: 2.6.1.1), alanine transaminase (ALT; EC: 2.6.1.2) and lactate dehydrogenase (LDH; EC: 1.1.1.27) and in the liver by depleted level of reduced glutathione (GSH), enhanced activity of glutathione peroxidase (GSH-Px; EC: 1I.11.1.9) and elevated level of lipid peroxides (LP). Captopril was given orally at three dose levels viz., 10, 25 and 50 mg/Kg/day for three consecutive days before subjecting the animals to the hepatotoxin. With the exception of the lowest dose namely, 10 mg/Kg/day, captopril afforded protection against CCl4-induced hepatotoxicity to different extents. Thus, the elevated activities of the enzymes AST, ALT, LDH and GSH-Px as well as the enhanced lipid peroxidation were markedly reduced below those elicited by the hepatotoxin, reaching values closer to the control, though still statistically higher. Captopril, however, did not ameliorate the depletion of GSH produced by CCl4. The data reported herein reveal a protective potential of captopril against the acute hepatotoxicity induced by CCl4 in mice. This hepatoprotection could be attributed, at least in part, to the free radical scavenging properties of the drug.
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PMID:Prior treatment with captopril attenuates carbon tetrachloride-induced liver injury in mice. 1209 Mar 55

Cocaine produces hepatotoxicity by a mechanism that remains undefined but that has been linked to its oxidative metabolism. Endotoxin (lipopolysaccharide, LPS) is also a well-known cause of hepatic damage, where exposure to non-injurious doses of LPS increases the toxicity of certain hepatotoxins. This study was conducted to investigate the possible potentiation of cocaine-mediated hepatotoxicity (CMH) by LPS. Male CF-1 mice were administered oral cocaine hydrochloride for 5 consecutive days at a dose of 20 mg/kg with and without 12 x 10(6) EU LPS/kg given intraperitoneally 4 h after the last cocaine injection. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured as markers of liver injury. Blood and liver glutathione (GSH) levels were determined, as well as the activities of glutathione peroxidase (GPx) and catalase (CAT). In addition, the activity of liver glutathione reductase (GRx) was measured. The results demonstrate that endotoxin potentiated the hepatotoxicity of cocaine. Serum ALT and AST were significantly elevated with the combined cocaine and LPS treatment versus all other treatments. While cocaine alone resulted in centrilobular necrosis, the cocaine and LPS combination produced submassive necrosis. The increased hepatic GSH content and GRx activity observed with cocaine alone were not observed with the combination treatment, rendering the liver more susceptible to oxidative stress. Moreover, there was a significant decrease in the activities of hepatic GPx and CAT, particularly with the combination treatment. In conclusion, this study demonstrates that LPS potentiates the hepatotoxicity of cocaine as revealed by an array of biochemical and morphological markers.
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PMID:Endotoxin potentiates the hepatotoxicity of cocaine in male mice. 1213 32

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