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)

A study was conducted on 60 broiler chicks of the effect of activated charcoal (200 ppm) on the toxicity of 0.5 ppm aflatoxin B1 (AFB1) in feed fed from day 1 to day 42. Activated charcoal was found to be moderately effective in reducing the harmful effects of AFB1 as assessed by growth response and various biochemical parameters. The feeding of activated charcoal along with AFB1 reduced the inhibitory effect of AFB1 on bodyweights and feed intake. There was also a significant improvement in the serum aspartate aminotransferase, alkaline phosphatase, total proteins, calcium and phosphorus levels. However, no significant improvement was observed in cholesterol levels.
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PMID:Toxicity of aflatoxin B1 in broiler chicks and its reduction by activated charcoal. 814 51

Administration of Aflatoxin B1 (AFB1) with safflower seed oil to hubbard chickens caused a significant increase in liver microsomal protein, electron transport components, and drug metabolizing enzymes. No alteration was observed in the activity of alanine and aspartate aminotransferases. AFB1 treatment with dimethylsulfoxide (DMSO) as a vehicle caused a significant decrease in electron transport components, drug metabolizing enzymes, and a significant increase in the activity of aspartate aminotransferase. Higher inhibition was observed at 1.5 mg/kg dose level of AFB1. Inhibition by AFB1 was maximal after 24 hr of treatment and decreased thereafter. AFB1 treatment with DMSO caused no significant change in electron transport components and drug metabolizing enzymes in Rhode Red Island (RRI) strain. Vancob male chickens showed significant decrease in electron transport components and drug metabolizing enzymes, while a significant increase was observed in vancob females. Results suggest that the effects of AFB1 depend on treatment vehicle, strain and sex of chickens.
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PMID:Effects of aflatoxin B1 on liver microsomal enzymes in different strains of chickens. 944 Feb 43

Although numerous studies report hepatic drug metabolizing enzyme alterations during aflatoxicosis, the mechanisms involved in P450 decreases remain to be established. The purpose of this work is to investigate whether increased oxidative damage revealed by the detection of malondialdehyde (MDA), lipofuscin substances, and conjugated dienes in microsomes, could explain the decreased P450 content. Studies were conducted with two different doses of aflatoxin B1 (AFB1), both in vivo in rabbits and ex vivo in primary cultures of rabbit hepatocytes, in the presence or absence of beta-naphthoflavone or rifampicin used as respective P450 inducers. Strong negative correlations were observed between MDA and P450 contents, both in vivo and ex vivo, whereas rifampicin appears to protect the hepatocytes from oxidative damage but not AFB1 toxicity. Positive correlation were also obtained between MDA formation and lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT) or alanine amino-transferase (ALAT) releases, used as non-specific markers of AFB1 toxicity. Taken together these results suggest that the dramatic decreases of cytochrome P450 observed in vivo during aflatoxicosis could be linked, at least in part, to microsomal oxidative damage.
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PMID:Cytochrome P450 decreases are correlated to increased microsomal oxidative damage in rabbit liver and primary cultures of rabbit hepatocytes exposed to AFB1. 1004 57

Aflatoxin B1, a metabolite of Aspergillus flavus is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B1-induced toxicity which could be mitigated by antioxidants. Many plant constituents, e.g. flavonoids, lignans and spice principles (capsaicin, curcumin, eugenol, etc.) have been reported to prevent liver damage associated with lipid peroxidation. In this study we investigated ternatin, a tetramethoxyflavone isolated from Egletes viscosa, for possible protection against liver injury induced by aflatoxin B1 in rats. Seventy two hours after a single intraperitoneal dose of aflatoxin B1 (1 mg kg(-1)), the concentration of malondialdehyde, the product of lipid peroxidation in liver homogenates, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly elevated (P<0.001). Subcutaneous ternatin (25 mg kg(-1)) pretreatment greatly reduced aflatoxin B1-induced increases in the levels of serum enzymes (ALT from 5071+/-763 to 293+/-66 international units L(-1) and AST from 4241+/-471 to 449+/-108 international units L(-1)) and elevated malondialdehyde levels (from 11.37+/-1.27 to 0.79+/-0.22 nmol (mg wet tissue)(-1)) in a manner similar to oral vitamin E (300 mg kg(-1)), a standard antioxidant. Further, histological changes induced by aflatoxin B1 such as hepatocellular necrosis and bile-duct proliferation were markedly inhibited in animals pretreated with ternatin or vitamin E. These data provide evidence that ternatin inhibits lipid peroxidation and affords protection against liver damage induced by aflatoxin B1. Ternatin might, therefore, be a suitable candidate for the chemoprevention of aflatoxicosis associated liver cancer.
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PMID:Inhibition by the bioflavonoid ternatin of aflatoxin B1-induced lipid peroxidation in rat liver. 1021 9

Aflatoxin B1 is an important consideration in the aetiology of human and animal hepatocellular carcinoma. The influence of the drug, Semecarpus anacardium Linn. nut extract, on hepatocarcinogenicity of aflatoxin B1 was evaluated in adult albino male Wistar rats. Aflatoxin B1 was administered intraperitoneally to induce hepatocellular carcinoma. These cancer bearing animals were treated with Semecarpus anacardium Linn. nut extract (200 mg/kg body weight/day) in sunflower oil orally for 14 days. The plasma and the liver tumour tissue were investigated biochemically for lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase. The elevation of plasma concentration of these enzymes were indicative of the persistent deteriorating effect of aflatoxin B1 in cancer bearing animals. Lactate dehydrogenase and aminotransferases levels were decreased in liver, whereas alkaline phosphatase and gamma-glutamyl transpeptidase were increased in cancer conditions. These enzyme levels were reversed to near normal control values in drug treated animals. The analysis of marker enzyme activities clearly indicates the antitumour efficacy of Semecarpus anacardium Linn. nut extract on aflatoxin B1 induced hepatocellular carcinoma.
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PMID:Anticancer potency of the milk extract of Semecarpus anacardium Linn. nuts against aflatoxin B1 mediated hepatocellular carcinoma bearing Wistar rats with reference to tumour marker enzymes. 1035 53

Acute aflatoxin B1 (AFB1)-induced hepatotoxicity was assessed in vivo in male Sprague-Dawley rats (150-300 g) using magnetic resonance imaging (MRI). MRI results were compared to serum enzyme levels, histology and electron microscopy. Twenty-four hours following intraperitoneal delivery of AFB1 (3 mg/kg body weight in a saline/dimethyl sulfoxide (DMSO; 0.03 ml/kg body weight) solution), regions of damage, characterised by increased proton signal intensities in T2-weighted images, were observed in the vicinity of the hepatic portal vein (HPV) and in the right medial regions of the liver. Image analysis of regions of apparent damage around the HPV and right medial regions, following 24 h of AFB1 exposure, indicated statistically significant (P<0.05) increases in proton image signal intensities, when compared to saline/DMSO-treated rats. No significant difference in proton image signal intensities were observed 1-2 h following AFB1 exposure. Twenty-four hours following AFB1 exposure, histopathological assessment was characterised by portal/central vein/artery congestion, sinusoid congestion, nuclear pyknosis and karyolysis, and hepatocyte vacuolation; electron microscopy (EM) examination indicated nuclear debris, swollen cytoplasmic compartments, vacuolation, and the disappearance of the smooth endoplasmic reticulum, and elevated levels of serum aspartate aminotransferase and alanine aminotransferase were found to be significantly different (P<0.01) than controls.
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PMID:Non-invasive in vivo magnetic resonance imaging assessment of acute aflatoxin B1 hepatotoxicity in rats. 1091 31

The effects of prolonged oral administration (21 days) of fumonisin B1 (FB1) and aflatoxin B1 (AFB1) were evaluated on male Wistar rats. The animals were housed in individual metabolic cages and submitted to the following treatments: 1-0 microg AFB1 + 0 mg FB1/100g bw.; 2-72 microg AFB1+ 0 mg FB1/100 g bw; 3-0 microg AFB1 + 0.5 mg FB1 g bw; 4-0 microg AFB1 + 1.5 mg FB1/100 g bw; 5-72 microg AFB1 + 0.5 mg FB1/100g bw; 6-72 microgAFB1 + 1.5 mg FB1/100g bw. On day 21, the rats were sacrificed for evaluation. The results showed that treated animals presented differences in body weight and absolute/relative weights of liver and kidney as well as altered hepatic function and cholesterol blood levels. Rats fed with the greatest doses of AFB1 and FB1 gained less weight (2.79 g/day) at the end of the experimental period; their blood concentrations of liver enzymes aspartate aminotransferase (AST) and alkaline phosphatase (AP) were above control levels (130.35 micro/l and 471.00 micro/l, respectively). Blood cholesterol increased in the groups treated with the highest dose of FB1 or FB1 associated with AFB1. Histopathology revealed the occurrence of apoptosis in the liver of rats exposed to FB1. The association of aflatoxin B1 with fumonisin B1 at higher dose probably potentiated the effects of the higher dose of fumonisin B1 acting singly.
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PMID:Effects of prolonged oral administration of fumonisin B1 and aflatoxin B1 in rats. 1150 59

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.
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PMID:Influence of ascorbic acid supplementation on the haematological and clinical biochemistry parameters of male rabbits exposed to aflatoxin B1. 1261 57

Hepatotoxic substances such as aflatoxin B1 (AFB1) produce free radical reactions during biotransformation damage to liver cells. Vitamins C and E are important natural antioxidants suppressing free radicals. This study investigated the effects of vitamins C and E on liver enzymes and other biochemical parameters in rabbits experimentally exposed to AFB1. The first group was control and fed the diet with dimethyl sulfoxide; the second group received 0.1 mg AFB1/kg diet; the third group received vitamin C (100 mg L-ascorbic acid/kg diet); the fourth group received vitamin E (100 mg alpha-tocopherol/kg diet); and the fifth group received vitamin C+vitamin E (100 mg L-ascorbic acid/kg diet+100 mg alpha-tocopherol/kg diet). Diets of the second, third, fourth and fifth groups were mixed with 0.1 mg AFB/kg diet) and feedings were continued for 10 w. Levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, creatine phosphokinase and lactate dehydrogenase after receiving AFB1 were significantly increased, while activities of aspartate transaminase, alanine transaminase, amylase, creatine phosphokinase and lactate dehydrogenase in groups receiving AFB1 + vitamins C, E or C+E were significantly lower than that of the AFB1-alone group. Although of the activity of alkaline phosphatase increased with AFB1 exposure, it decreased with vitamin C administration. Levels of urea, triglyceride, cholesterol and albumin were affected by AFB1 and AFB1+vitaminC. AFB1 affected some liver enzymes and other biochemical parameters, but vitamins C, E and C+E partially prevented an increase in these liver enzymes and some the biochemical parameters induced by AFB1.
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PMID:Effects of vitamin C and E on liver enzymes and biochemical parameters of rabbits exposed to aflatoxin B1. 1530 90

To elucidate the potential factors modulating exposure to aflatoxin B1 (AFB1) in three Chinese populations, an epidemiologic study was conducted in Fusui County and Nanning City of Guangxi Province and Chengdu City of Sichuan Province. The incidence rates of hepatocelluar carcinoma (HCC) for males in these three regions were 92-97 per 100,000, 32-47 per 100,000, and 21 per 100,000, respectively. Eighty-nine residents from Fusui, 196 residents from Nanning, and 118 residents from Chengdu were screened for AFB1-albumin adduct (AAA) levels and hepatitis virus (HBV, HCV, HDV, HEV, and HGV) infections, as well as liver biochemistry (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], y-glutamyl transpeptidase [GGT], 5'-nucleotidase, globulin [GLO], direct bilirubin, indirect bilirubin, and bile acid levels). At least one marker of hepatitis virus (HV) infection was present in 47.2% (42/89) of subjects from Fusui, while in Nanning and Chengdu the values were 15.8% (31/196) and 22.0% (26/118), respectively. In contrast to females, a higher level of AAA was observed in males; the difference was statistically significant in both the Nanning (P = 0.023) and the Chengdu (P = 0.026) subjects. In the Chengdu group, there was a significantly higher level of AAA in cases with HV infection (P = 0.041). There was a close association between AAA level and BMI in the adults without HV infection (r = 0.148, P = 0.044). Also, AAA was closely associated with DBIL and GGT in non-HV-infected minors (P < 0.05), closely associated with ALB, GLO, and GGT in HV-infected minors (P < 0.05), and closely associated with IBIL, GLO, TBA, and AST in non-HV-infected adults (P < 0.01). The co-effect of HV infection and AFB1 exposure may be responsible for the high risk of HCC in the Fusui region, whereas age, gender, BMI, and HV infection may modify individual aflatoxin levels. The relationship between AAA level and liver biochemistry indicates injury induced by aflatoxin to both hepatic parenchyma and biliary tract. But the associations vary with age and HV infection status.
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PMID:Associated factors in modulating aflatoxin B1-albumin adduct level in three Chinese populations. 1581 Jun 36


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