Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol pretreatment has the potentiation of the aflatoxin B1-induced hepatotoxicity was indicated by an increase in the activities of plasma GPT, plasma GOT and in the severity of liver necrosis. The effect of ethanol pretreatment on an increase in the accumulation of liver triglycerides is additive in nature.
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PMID:Aflatoxin B1 hepatotoxicity in rats pretreated with ethanol. 66 55

1. Aflatoxin B1 (1.5 mg/kg body weight, i.p.) was administered to rats, mice, quail and chickens to examine the comparative effect on hepatic microsomal drug-metabolizing enzymes, cytosolic glutathione S-transferase and serum enzymes. 2. Administration of aflatoxin B1 to rats resulted in a significant decrease in microsomal cytochrome P-450, NADPH-cytochrome c reductase, activities of aminopyrine N-demethylase, aniline hydroxylase, cytosolic glutathione S-transferase and liver glutathione content. However, no significant changes in these parameters were seen in mice. 3. Quail showed a significant decrease in the content of cytochrome P-450 and the activities of aminopyrine N-demethylase, aniline hydroxylase and cytosolic glutathione S-transferase. A similar treatment did not affect these biotransformation enzymes in chickens. 4. The activities of serum enzymes, sorbitol dehydrogenase, alanine aminotransferase and aspartate aminotransferase were increased significantly in rats and quail. Mice exhibited a significant increase in the activities of sorbitol dehydrogenase and aspartate aminotransferase, while chickens showed a significant increase only in alanine aminotransferase.
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PMID:Comparative assessment of the effect of aflatoxin B1 on hepatic dysfunction in some mammalian and avian species. 135 19

The effects of crocetin pretreatment on both hepatic aflatoxin B1 (AFB1)-DNA binding and AFB1 hepatotoxicity in rats has been examined. For these studies, male Wistar rats were treated with AFB1 (2 mg/kg) by i.p. administration, and the different degrees of hepatic damage were revealed by the elevations of levels of serum marker enzymes such as aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and gamma-glutamyltranspeptidase. After pretreatment of the animals with crocetin (2 or 6 mg/kg) daily for three consecutive days, the enzyme elevations were significantly suppressed. This suggested that the crocetin possessed chemopreventive effects on the early acute hepatic damage induced by AFB1. Under these experimental conditions, consistent elevations of hepatic glutathiones (GSH) and activities of glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) were observed. Crocetin treatment also decreased AFB1-DNA adduct formation in AFB1-treated animals. From these results, we suggest that the protective effect of crocetin on AFB1 hepatotoxicity in rats might be due to the hepatic tissues' defense mechanisms that elevated the cytosol GSH and the activities of GST and GSH-Px.
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PMID:Effects of crocetin on the hepatotoxicity and hepatic DNA binding of aflatoxin B1 in rats. 167 27

Subacute doses (1/20 LD50) of aflatoxin B1 and ochratoxin A were fed to weanling albino rats individually and in combination for 36 weeks and then rats were maintained on toxin free normal diet for a period of 24 weeks. Livers of rats were fatty, wherever aflatoxin was administered but the enzyme activity did not show significant differences among various groups. However, in a few individuals whose livers were severely affected, higher concentrations of urine creatinine, liver RNA and DNA, and ALT enzyme activity were recorded. Histopathological examination showed various stages of hepatoma and hepatocarcinoma including nodular hyperplasia, hypertrophy, vacuolisation, degeneration, pseudolobulation, cellular infiltration and fibrosis of liver of rats fed with aflatoxin individually and in combination. Few anaplastic cells in the corticomedullary region and nuclear enlargement of proximal tubular epithelium of kidney were found wherever combined toxin and ochratoxin alone were administered. Liver tumor expression was time dependent.
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PMID:Effect of long term feeding and withdrawal of aflatoxin B1 and ochratoxin A on kidney cell transformation in albino rats. 179 62

The suppressive effects of crocetin (a natural carotenoid) on the hepatotoxic lesions induced by aflatoxin B1 (AFB1) were investigated in male Wistar rats. Rats were divided into five groups: groups I and II served as normal and solvent control respectively. Group III was given AFB1 (25 micrograms/day/rat) alone; group IV was given crocetin (0.1 mg/day/rat) alone; and group V received both AFB1 and crocetin. Rats received AFB1 and crocetin for 9 and 10 weeks respectively, and were maintained on basal diet for 35 weeks. At the end of the experiment (week 45), the incidence of liver lesions in rats of group V was significantly reduced by approximately 40% compared with group III. There were no liver lesions in rats of groups I, II and IV. A significant protective effect of crocetin on AFB1 hepatotoxicity was shown, as manifested by reduced effects on the activities of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase (P less than 0.01-0.001). From our previous results and present data, we suggest that the suppression of crocetin on AFB1 hepatotoxicity in the rats might be due to the defense mechanisms of hepatic tissues that elevated the GSH S-transferase activity and decreased the formation of hepatic AFB1-DNA adducts.
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PMID:Suppression of aflatoxin B1-induced hepatotoxic lesions by crocetin (a natural carotenoid). 193 61

This study characterized the effects of liver damage produced by a variety of hepatotoxicants on several components of the sulfation pathway in rats. Specifically, the concentration of cosubstrate, adenosine 3'-phosphate 5'-phosphosulfate (PAPS), and the hepatic capacity for PAPS synthesis were measured in livers of rats treated with carbon tetrachloride (CCl4), 1,1-dichloroethylene (DCE), alpha-naphthylisothiocyanate (ANIT), aflatoxin B1 (ATX), allyl alcohol (AA), bromobenzene (BB), cadmium chloride (Cd), or thioacetamide (TA). Liver damage was assessed by measuring serum sorbitol dehydrogenase (SDH) and alanine aminotransferase (ALT) activities as well as by histopathological examination. Hepatic PAPS concentration was generally decreased as a result of treatment with hepatotoxicants (35-80% of control), although BB, AA, and ANIT were without effect. Maximal hepatic capacity for PAPS synthesis, determined as the activities of PAPS synthetic enzymes, ATP sulfurylase, and APS kinase, was selectively decreased by the hepatotoxicants. ATP sulfurylase activity was decreased by Cd and TA (55 and 62% of control, respectively), whereas APS kinase activity was decreased by Cd, TA, BB, and DCE (60-77% of control, respectively). In addition, phenol sulfotransferase (PST) activity was measured toward 1- and 2-naphthol in order to determine whether apparent changes in PST activity in damaged livers are substrate-dependent. Treatment with hepatotoxicants generally decreased 1-naphthol-directed PST activity but not PST activity directed toward 2-naphthol. In conclusion, (1) not all xenobiotic-induced liver injury results in decreased hepatic PAPS concentration, (2) some hepatotoxicants decrease PAPS concentration by a mechanism other than decreased cosubstrate synthesis, and (3) the effect of hepatotoxicants on PST activity is dependent upon the choice of substrate used in the enzymatic assay.
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PMID:The differential effects of hepatotoxicants on the sulfation pathway in rats. 194 7

The early effects (60 min) of aflatoxin B1 (AFB1) on membrane permeability and carbohydrate metabolism of liver cells were studied in fresh suspensions of rat hepatocytes. Evaluation by trypan blue exclusion, enzyme leakage, glycogen synthesis or degradation, and glyconeogenesis were chosen as viability tests. The results obtained showed an increase of lactate dehydrogenase (LDH), alanine aminotransferase (GPT) and aspartate aminotransferase (GOT) released into the medium and also an increase in the number of stained cells. These changes were significant at about 18 nmol/10(6) cells of AFB1, while a remarkable effect of the toxin on glyconeogenesis and glycogen synthesis or degradation was observed at 9 nmol/10(6) cells, doses commonly used for in vitro studies.
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PMID:Early influence of aflatoxin B1 on the functional state of isolated rat hepatocytes. 249 69

Chemopreventive agents are compounds that inhibit carcinogenesis when administered prior or subsequent to a course of carcinogen administration. The effects of dietary administration of crocin dyes on the hepatic damage induced by aflatoxin B1 (AFB1) and dimethylnitrosamine (DMN) in rats were investigated. Female Sprague-Dawley rats were treated with different dosages of AFB1 (0.9 or 4.5 mg/kg) or DMN (8 or 20 mg/kg) by i.p. administration, and the different degrees of hepatic damage were revealed by the elevations of levels of serum marker enzymes such as aspartate amino-transferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and lactic dehydrogenase. Pre-treatment of the animals with crocin dyes 50 mg/kg daily for three consecutive days, the enzyme elevations were significantly suppressed. This suggested that the crocin dyes possessed chemopreventive effects on the early acute hepatic damage induced by AFB1 or DMN. Feeding experiments demonstrated that crocin dyes at 0.1% in the diet could suppress partially the chronic hepatic damage induced by multiple dosages of AFB1 or DMN, but at a higher concentration of 1% crocin dye failed to do so because of their host toxicity. Crocin dyes are extracted from the fruits of Gardenia jasminoides and consist of carotenoids and geniposides as active principles. The protective mechanisms of crocin dyes may be attributed to their carotenoids which are converted metabolically to retinoids in rats.
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PMID:Protection of crocin dyes on the acute hepatic damage induced by aflatoxin B1 and dimethylnitrosamine in rats. 287 Aug 20

The interaction of ethanol and aflatoxin B1 (AFB1)-induced hepatotoxicity was studied in male Wistar rats using the activity of plasma GOT and GPT, liver triglyceride and histopathologic changes of liver necrosis as indices. Pretreatment of four oral doses of ethanol (4.0 g/kg BW each) at 48, 45, 24 and 21 hrs prior to AFB1 (0.5 to 2.0 mg/kg BW) single i.p. administration caused a significant increase in the activity of PGOT (6 folds) and PGPT (5 folds), liver triglycerides (2 folds) and severity of liver necrosis at 48 hrs after AFB1 administration. Ethanol pretreatment potentiated AFB1-induced hepatotoxicity by increasing MFO enzymes, aniline hydroxylase and p-nitroanisole-O-demethylase activity and lipid peroxidation, and decreasing in cytochrome b5, epoxide hydrolase activity and hepatic glutathione content. However, it did not cause any significant change in the activity of NADPH-cytochrome c reductase and glutathione-S-transferase and cytochrome P-450. These results suggest that potentiation of ethanol pretreatment on AFB1-induced hepatotoxicity may be due to an increase in the metabolic formation of AFB1-2, 3-oxide and subsequent binding to DNA.
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PMID:Potentiation of aflatoxin B1 induced hepatotoxicity in male Wistar rats with ethanol pretreatment. 308 65

Studied were some paraclinical indices of the blood of 50 broiler birds treated with aflatoxin B1. It was found that the effect of the mycotoxin used in concentrations of 25.0 and 37.5 micrograms in the course of thirty days and in conc. of 50.0 micrograms in the course of five days with three test groups of birds (as compared to a group of controls) consisted in the drop of total protein and the rise of the activity of GOT, GPT, and total bilirubin. It was demonstrated that the use of feeds containing aflatoxin B1 had a bearing on the microbiologic status of the meat and liver. There was no increase in the total count of aerobic mesophile organisms.
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PMID:[Paraclinical research on broiler chickens treated with aflatoxin B1 and microbiological studies of the meat and liver obtained from them]. 393 26


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