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

Exposure of human plasma in vitro to gas-phase cigarette smoke (CS) causes a marked modification of plasma proteins as measured by protein carbonyl assay. Aldehydes present in CS may cause this elevation of protein carbonyls by reacting with sulfhydryl groups of proteins. Saliva is the first body fluid to confront the inhaled CS. Thus, in vitro exposure of saliva to nine "puffs" of CS also showed a distinct increase in protein carbonyls. Ascorbate and desferrioxamine mesylate had little effect on protein carbonyl formation, while GSH and N-acetylcysteine considerably inhibited the accumulation of protein carbonyls due to CS exposure. Following the exposure to CS, the activities of several salivary enzymes-amylase, lactic dehydrogenase (LDH), and acid phosphatase-were found to be significantly reduced (34, 57, and 77%, respectively). However, CS had no effect on the activities of aspartate aminotransferase and alkaline phosphatase. Addition of 1 mM of GSH and N-acetylcysteine considerably protected LDH and amylase activities, suggesting that sulfhydryl groups are affected in LDH and amylase. On the other hand, addition of 1 mM ascorbate caused a further loss of LDH and amylase activities, which could be partially prevented by the addition of desferrioxamine mesylate, implicating metal-catalyzed oxidation processes. Finally, loss of acid phosphatase activity was completely unaffected by any of the above antioxidants. It is concluded that the loss of salivary enzyme activities may be due to various agents in the CS that affect the enzyme activities via different mechanisms.
 ...
PMID:Effect of cigarette smoke on salivary proteins and enzyme activities. 1089 39

Exercise-induced free-radical production may be partly responsible for muscle soreness and damage following demanding exercise. A number of studies have investigated the effect of antioxidant supplementation although there is a paucity of information regarding vitamin C. Therefore the aim of the present study was to investigate the effect of vitamin C supplementation on exercise-induced muscle soreness and damage. Nine habitually active males consumed a 1 g dose of vitamin C 2 h before exercise, and on another occasion consumed an identical placebo. The exercise comprised a 90 min intermittent shuttle-running test, which was designed to simulate the multiple-sprint sports. Vitamin C supplementation increased plasma concentrations of vitamin C before exercise, and plasma concentrations continued to increase during the shuttle-run to reach a peak of approximately 200 micromol x l(-1) immediately after exercise. However, muscle soreness, and markers of both muscle damage (creatine kinase and aspartate aminotransferase) and lipid peroxidation (malondialdehyde) were elevated to an equal extent after exercise in placebo and supplemented trials. Therefore acute supplementation with vitamin C had no beneficial effects although it is possible that such short-term vitamin C supplementation was ineffective because it occurred at an inappropriate time.
 ...
PMID:Muscle soreness and damage parameters after prolonged intermittent shuttle-running following acute vitamin C supplementation. 1125 44

This study was undertaken to evaluate the effectiveness of L-ascorbic acid (AA) in alleviating the toxicity of aflatoxin B1 (AFB1) in male New-Zealand white rabbits. Five rabbits (6 months of age and mean body weight 3.12 kg) per group were assigned to 1 of 6 treatment groups: 0 mg AA and 0 mg AFB1/kg BW (control); 20 mg AA/kg BW; 15 microg AFB1/kg BW; 15 microg AFB1 plus 20 mg AA/kg BW; 30 pg AFB1/kg BW; 30 pg AFB1 plus 20 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 9 weeks, followed by a 9-week recovery period where all drugs were withdrawn. Evaluations were made for hemato-biochemical parameters and enzymatic activities. Results showed that AFB1 significantly (p < 0.05) decreased hemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), in a dose-dependent manner, and these effects were continued during the recovery period. Ascorbic acid caused an increase in these parameters, and alleviated the negative effect of AFB1 during the treatment period. Additionally, serum concentrations of total protein, albumin and glucose were significantly (P < 0.05) declined by treatment with the high dose of aflatoxin and these effects were continued during the recovery period. Ascorbic acid caused non-significant increases in these parameters and alleviated the harmful effect of AFB1. On the other hand, aflatoxin treatment caused significant increases (P < 0.05) in the activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (AlP) during the treatment period in a dose dependent manner, and this effect was continued during the recovery period, especially with the high dose. Also, treatment with the high dose of aflatoxin caused significant increases (P<0.05) in cholesterol and total bilirubin. Ascorbic acid caused significant decreases in these parameters and alleviated the harmful effects of AFB1. Whereas, Total leukocyte count (TLC), urea and creatinine were not significantly affected by aflatoxin-treatment. Generally, it is interesting feature that the treatment with AA alone had no negative effects on most of the previous parameters. Also, the presence of AA could diminished the adverse effects of AFB1 on most of hematological and biochemical values, and enzymatic activities in rabbits.
 ...
PMID:Influence of ascorbic acid supplementation on the haematological and clinical biochemistry parameters of male rabbits exposed to aflatoxin B1. 1261 57

The effects of cadmium on performance, antioxidant defense system, liver and kidney functions, and cadmium accumulation in selected tissues of broiler chickens were studied. Whether the possible adverse effects of cadmium would reverse with the antioxidant ascorbic acid was also investigated. Hence, 4 treatment groups (3 replicates of 10 chicks each) were designed in the study: control, ascorbic acid, cadmium, and cadmium plus ascorbic acid. Cadmium was given via the drinking water at a concentration of 25 mg/L for 6 wk. Ascorbic acid was added to the basal diet at 200 mg/kg either alone or with cadmium. Cadmium decreased the body weight (BW), body weight gain (BWG), and feed efficiency (FE) significantly at the end of the experiment, whereas its effect on feed consumption (FC) was not significant. Cadmium increased the plasma malondialdehyde (MDA) level as an indicator of lipid peroxidation and lowered the activity of blood superoxide dismutase (SOD). Liver function enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma glutamyl transferase (GGT) activities were not changed by cadmium. Cadmium ingestion did not alter serum creatinine levels. Although the serum cadmium level was not elevated, cadmium mainly accumulated in the kidneys, liver, pancreas, and muscle. Ascorbic acid supplementation resulted in a reduction of MDA level previously increased by cadmium and a restoration in SOD activity. However, ascorbic acid did not ameliorate the growth inhibitory effect of cadmium nor did it prevent accumulation of cadmium in analyzed tissues. These data indicate that oxidative stress, induced by cadmium, plays a role in decreasing the performance of broilers and that dietary supplementation by ascorbic acid might be useful in reversing the lipid peroxidation induced by cadmium and partly alleviating the adverse effect of cadmium on performance of broilers.
 ...
PMID:Effects of ascorbic acid on cadmium-induced oxidative stress and performance of broilers. 1585 29

Halothane is an important human and veterinary anesthetic, which produces free radicals during biotransformation. Occasionally, these free radicals may cause hepatic injury, especially in case of multiple halothane exposures over short periods. Vitamin C may protect cellular lipids and lipoproteins against oxidative damage by the free radicals. This study investigated the effects of vitamin C on liver enzymes and other biochemical parameters in rats anesthetized with halothane. One group of rats was used as a control, and saline (0.9% NaCl) was injected intraperitoneally into these animals as a placebo. The second group of rats was used as an anesthesia control group and was only anesthetized by halothane for 2 h. The third group was anesthetized by halothane and injected vitamin C intraperitoneally. Activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase enzymes were significantly increased (p < 0.05, p < 0.01, p < 0.05, respectively) by halothane anesthesia, but decreased (p < 0.05, p < 0.05, p < 0.05, respectively) with administration of vitamin C. Concentrations of triglycerides, cholesterol, total bilirubin and creatinine were statistically affected (p < 0.05, p < 0.01, p < 0.05, and p < 0.01, respectively) by injection of vitamin C. Values of erythrocyte counts, packet cell volumes, hemoglobin concentration, leukocyte counts, rates of neutrophils and lymphocytes were significantly affected (p < 0.01, p < 0.05, p < 0.05, p < 0.01, p < 0.001 and p < 0.01, respectively) by halothane anesthesia. The values of erythrocyte counts, leukocyte counts, neutrophil and lymphocyte rates were significantly decreased (p < 0.05, p < 0.05, p < 0.05, p < 0.01 and p < 0.01, respectively) with administration of vitamin C. Based upon these results, vitamin C may play an important role in the prevention of hepatic cellular injury inflicted by halothane anesthesia.
 ...
PMID:Effects of vitamin C on liver enzymes and biochemical parameters in rats anesthetized with halothane. 1590 86

Aluminium (Al) has been proposed as an environmental factor that may contribute to some diseases, affect several enzymes and other biomolecules and induced free radical-mediated cytotoxicity. Also, Al induced reproductive toxicity and exerted a significant adverse effect on the steroidogenesis. The antioxidant ascorbic acid (AA) plays an important role in various physiological processes in the body including detoxification of different toxic materials. Therefore, the present investigation aimed to elucidate possible protective effects of AA in alleviating the toxicity of aluminium chloride (AlCl3) on reproductive performance, lipid peroxidation and enzyme activities in seminal plasma of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg AA and 0 mg AlCl3 /kg body weight (BW) (control); 40 mg AA/kg BW; 34 mg AlCl3 /kg BW; 34 mg AlCl3 plus 40 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Results obtained showed that AlCl3 significantly (P<0.05) decreased libido (by increasing the reaction time), ejaculate volume, sperm concentration, total sperm output, sperm motility (%), total motile sperm per ejaculate (TMS), packed sperm volume (PSV), total functional sperm fraction (TFSF), normal and live sperm and semen initial fructose. While initial hydrogen ion concentration (pH) and dead and abnormal sperm were increased (P<0.05). Live body weight (LBW), feed intake (FI) and relative weights of testes (RTW) and epididymis (REW) were significantly (P<0.05) decreased. Concentrations of thiobarbituric acid-reactive substances (TBARS) were significantly (P<0.05) increased in seminal plasma of rabbits treated with AlCl3 compared with control. While, activities of glutathione S-transferase (GST), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and acid phosphatase (AcP) were significantly (P<0.05) decreased. Ascorbic acid alone significantly increased LBW, FI, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of free radicals. Also, the present study showed that ascorbic acid might be effective in the protection of aluminium-induced reproductive toxicity. It was suggested that AlCl3 exerted a significant adverse effect on reproductive performance of male rabbits. Furthermore, AA could be able to antagonize the toxic effects of AlCl3 and improved semen quality of male rabbit.
 ...
PMID:Aluminium-induced deterioration in reproductive performance and seminal plasma biochemistry of male rabbits: protective role of ascorbic acid. 1609 53

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).
 ...
PMID:Changes in biochemical parameters in rabbits blood after oral exposure to diphenyl diselenide for long periods. 1673 89

In the present study, preventive and protective effects of Ocimum gratissimum in ethanol-induced hepatotoxicity are assessed in albino rats. A methanol extract of O. gratissimum leaves is prepared, with a yield of 3.5% (w/w) of the dry weight of leaves. Graded doses of the extract (10, 20, 40 and 80 mg/kg body weight), together with ethanol (5 gm/kg body weight) are administered orally to experimental groups for 30 days. Normal control rats receive distilled water only, while rats in an alcohol control group (AC) receive ethanol only for 30 days. O. gratissimum reduced the level of thiobarbituric acid reactive substance in all experimental groups (E1-E4). Alanine transaminase and aspartate transaminase levels fell in all experimental groups (E1-E4), but this reduction was significant only in groups E3 and E4 (P < 0.05), indicating inhibition of lipid peroxidation by free radicals generated after ethanol metabolism. Levels of antioxidants also increased. Ascorbic acid and glutathione levels increased in all experimental groups (E1-E4; P < 0.05 and P < 0.01, respectively). A significant increase in catalase (P < 0.05) was noted only in group E4, although an upward trend was noted in all experimental groups. This study shows that O. gratissimum prevents free radical damage to the liver and thus protects the organ from oxidative stress.
 ...
PMID:Preventive and protective effects of wild basil in ethanol-induced liver toxicity in rats. 1744 12

Chlorpyrifos (CPF) is one of the most widely used organophosphorous insecticides in agriculture with its attendant adverse health outcomes. This study aimed at evaluating the effect of subchronic oral CPF administration on hematological and serum biochemical indices, and the possible ameliorating effect of vitamin C on the indices in mice. Thirty mice divided into 3 groups of 10 mice each were used for this study. Mice in group I (control) were dosed with vegetable oil, while those in group II were given CPF (21.3 mg/kg~ 1/5(th) LD(50)) only. Mice in group III were pretreated with vitamin C (100 mg/kg) prior to dosing with CPF 30 min later (Vitamin C + CPF-treated group). This regime was given to each group of mice three times a week for a period of ten weeks. During the study period, mice were examined for signs of toxicity, and weight of each mouse was measured every week. At the end of the study period, blood samples were collected from the mice and analyzed for packed cell volume (PCV), total red blood cell (RBC), white blood cell (WBC) and total protein (TP). Serum obtained from the blood was analyzed for Na( +, K+ and Cl-), urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The results showed that mice in the vitamin C + CPF-treated group exhibited milder signs of toxicity and significant increase in weight gain (p<0.01) compared to the CPF-treated group. No significant increase in weight in the CPF-treated group was observed compared to the control. There was a significant increase in PCV, RBC, Hb, TP and creatinine, but a significant decrease was obtained in WBC, ALT and AST in the CPF-treated group compared to the control. All the parameters with the exception of WBC, ALT and AST (which increased significantly), were significantly decreased in the vitamin C + CPF-treated group compared to CPF-treated group. ALP was significantly elevated in the CPF-treated group compared to both the control and vitamin C + CPF-treated group. No significant changes in urea and the measured electrolytes in all three groups, except a significant decrease in the concentration of Na(+) was observed in the CPF-treated group compared to the control. The study demonstrated that pretreatment of CPF-administered mice with vitamin C significantly altered some important hematological and serum biochemical parameters, revealing the protective action of the vitamin against some organ damage induced by CPF.
 ...
PMID:Evaluation of subchronic chlorpyrifos poisoning on hematological and serum biochemical changes in mice and protective effect of vitamin C. 1753 35

Excess hepatic iron generates reactive oxygen species that result in oxidative stress and oxidative damage to the liver. Vitamins have hitherto been considered to be a possible remedy. The aim of this study was to determine if high doses of delta-alpha-tocopherol supplementation in iron overload would ameliorate the oxidative stress. Four groups of 20 male Wistar albino rats were studied: group 1 (control) was fed normal diet, group 2 (Fe) 0.75% Ferrocene iron, group 3 (FV gp) 0.75% Ferrocene/delta-alpha-tocopherol (10x RDA), group 4 (V gp) normal diet/delta-alpha-tocopherol. After 12 months, serum iron, reduced glutathione, catalase, vitamin C, Oxygen Radical Absorbance Capacity, lipid peroxidation, 8-hydroxy-2'-deoxyguanosine (8-OHdG), aspartate transaminase (AST), and alanine transaminase (ALT) were measured. Vitamin C levels were: F gp = 5.04 +/- 0.09; FV gp = 5.85 +/- 0.13 (micromol/l) (p < 0.05). 8-hydroxy-2'-deoxyguanosine levels were: F gp = 143.6 +/- 6.4; FV gp = 179.2 +/- 18.2 (ng/ml) (p < 0.05). Oxidative liver damage, as determined by serum AST and ALT levels, was not attenuated by alpha-tocopherol. A positive correlation existed between vitamin C and 8-OHdG, suggesting possible delta-alpha-tocopherol toxicity.
 ...
PMID:Possible adverse effect of high delta-alpha-tocopherol intake on hepatic iron overload: enhanced production of vitamin C and the genotoxin, 8-hydroxy-2'- deoxyguanosine. 2010 38


1 2 3 Next >>