Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aflatoxin carcinogenesis appears to relate to multiple factors. This includes bulky adduct formation at DNA guanine N-7. The process also requires more extensive physiological degradation, possibly by the toxin alone as the active principle, but in instances also involving other assaults (e.g., hepatitis B virus). Since aflatoxin carcinogenesis involves complex effects, we have undertaken to define the range of influence of this common food contaminant upon a susceptible model, the broiler-type chick. Aflatoxicosis in two treated groups was indicated by jaundice, coagulopathy, dehydration of combs and shanks, retardation of body weight, and decrease in bursa weight. Blood clotting time, hemoglobin content, erythrocyte and packed-cell volume were affected. Hepatocytes were swollen and had undergone fatty degeneration. Bile duct hyperplasia was evident. Total serum protein, alkaline phosphatase, creatine, lactate dehydrogenase, serum glutamic oxalacetic transaminase and glutamyl transpeptidase were similarly abnormal in birds receiving the contaminated (0.5 and 2.5 micrograms/g aflatoxin B1) feed rations. The aflatoxin B1 and its metabolites were isolated by HPLC from chick serum, liver and muscle.
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PMID:Clinical and biochemical effects of aflatoxin in feed ration of chicks. 392 39

Sixteen clinically normal, healthy ponies were randomly assigned to 4 groups and given aflatoxin B1 in doses of 0.045, 0.030, 0.015, and 0 (control) mg/kg of body weight per day for 21 days (or total doses of 0.945, 0.630, 0.315, and 0 mg/kg). The animals were allowed to recover for 3 months and then were reassigned to 4 treatment groups such that each group during the 2nd trial included a pony from each of the groups of the 1st trial. The animals in the new groups were intubated and were given aflatoxin in doses of 0.4, 0.2, 0.1, and 0 (control) mg/kg/day for 5 days ( or total doses of 2.0, 1.0, 0.5, and 0 mg/kg). Venous blood samples were drawn every other day to monitor for toxicosis; examinations were made for RBC and WBC counts, hemoglobin concentration, PCV, serum urea nitrogen, prothrombin time, and serum concentrations of aspartate aminotransferase, iditol dehydrogenase, alkaline phosphatase, albumin, gamma-glutamyl transferase, and arginase. There were no significant differences between treatment groups and controls (given no aflatoxin) in the toxicologic values examined for during the 1st trial. During the 2nd experiment, 2 of the ponies in the large-dose treatment gorup (2.0 mg/kg) demonstrated increased serum enzyme activities. These animals had been in the large-dose (0.945 mg/kg) and median-dose (0.63 mg/kg) groups during the 1st trial. Arginase, iditol dehydrogenase, and gamma-glutamyl transpeptidase activities became increased on the 4th day of treatment and continued to increase until the 6th day of the experiment (1 day after treatment was terminated). These enzymes approached control group values at 10 days after cessation of treatment. These increases were indicative of hepatocellular toxicity. It was concluded that the possibility of equine aflatoxicosis exists although ponies given high quality rations appear to be less susceptible than some other species. Prior exposure to aflatoxins may predispose to clinical toxicity on subsequent exposure, despite lack of expression of clinical signs.
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PMID:Effects of aflatoxins in young ponies. 612 12

The effects of chronic intra-peritoneal administration of aflatoxin B1 on the activity of alkaline and acid phosphatases; glutamic oxaloacetate (GOT) and pyruvate transaminases (GPT); 5'-nucleotidase and lactic dehydrogenase enzymes were monitored in the testis and kidney of adult albino rats. Results showed that aflatoxin B1 depressed the activity of alkaline phosphatase in both tissues, but increased that of acid phosphatase in only the testis. While GOT and 5'-nucleotidase were inhibited, GPT and lactic dehydrogenase activity was enhanced by this carcinogen. These responses were similar for the testis and kidney. The above findings coupled with the microscopical observation of the testis tissue seem to indicate that the essential lesion of this toxin on the testis may be a modification of the enzymes of germinal cells resulting from a gradual depletion of the latter. Furthermore, the results appear to show that by and large, aflatoxin B1 exerts only slightly different effects on the testis and kidney at the enzyme level.
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PMID:The effects of aflatoxin B1 on some testicular and kidney enzyme activity in rat. 625 8

Groups of 8 male crossbreed domestic goats were given 3 dosage levels of aflatoxin B1 [(AFB1) mg/kg of body weight/day] orally: 0.1 for 34 days; 0.2 for 18 days; or 0.4 for 10 days. Clinical condition, feed consumption, and selected blood values were determined. Clinical signs of toxicosis included decreased feed consumption, slight-to-moderate loss of body weight, mucopurulent nasal discharge, dyspnea, coughing, lethargy, icterus, diarrhea (4 goats), and subnormal body temperature 24 to 48 hours before death. Clinicopathologic changes included increases in total RBC count, PCV, hemoglobin concentration, serum bilirubin concentration, and serum activities of aspartate aminotransferase, isocitric dehydrogenase, and ornithine carbamyl transferase. Goats given the 2 smaller dosage levels of AFB1 had slight increases of serum total protein (TP) concentration compared with control goats, but goats given the larger dosage levels of AFB1 initially had a slight decrease in TP. Aflatoxin had little effect on total WBC count. Serum alanine aminotransferase (ALT) activities in goats given the 2 larger dosage levels of AFB1 were similar to those of control goats, but goats given the smallest dosage level of AFB1 had increased serum ALT activities. Aflatoxin did not produce consistent dose-related changes in serum alkaline phosphatase activities. Seemingly, goats are susceptible to aflatoxin. Onset of clinical signs was dose-related. Onset and magnitude of increases in PCV, hemoglobin concentration, serum bilirubin concentration, and activities of serum aspartate aminotransferase, ornithine carbamyl transferase, and isocitric dehydrogenase were dose-related. Changes in TP and activities of serum ALT and alkaline phosphatase were neither dose-related nor were they potentially useful indicators of toxicosis.
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PMID:Caprine aflatoxicosis: experimental disease and clinical pathologic changes. 643 Jan 34

When aflatoxin-contaminated grain is consumed by dairy cows, aflatoxin M1 is excreted in the milk. Sixteen neonatal male Holstein calves were given milk which had been collected from cows given 5 to 6 mg of aflatoxin B1 each day. The calves were examined for possible detrimental effects of the mycotoxin at pseudophysiologic concentrations. Calves were allotted to 1 of 4 groups given different milk dietary aflatoxin M1 concentrations: group 1--given 0 microgram of aflatoxin M1/L (undetectable); group 2--given 0.5 microgram/L; group 3--given 1 microgram/L; and group 4--given 2 micrograms/L. Whole milk equal to 8% of body weight was fed daily and adjusted each week to maintain this ratio. Water and a 15% crude protein complete calf starter ration were offered ad libitum for the 6-week feeding study. Weekly blood samples were collected via jugular venipuncture and analyzed for serum alkaline phosphatase and aspartate aminotransferase activities. Daily means for milk dry matter intake (in kg) and complete ration intake (in kg) for the calf groups were as follows: 0.46 and 0.36 for group 1; 0.46 and 0.25 for group 2; 0.42 and 0.18 for group 3; and 0.49 and 0.40 for group 4. Significant differences in complete ration and total dry matter intake were noted. The average daily gains (in kg) and gains in height at withers (in cm) were 0.39 and 4.1 for group 1; 0.36 and 4.0 for group 2; 0.29 and 5.7 for group 3; and 0.42 and 5.1 for group 4.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of aflatoxin M1 intake at physiologic levels on newborn dairy calves. 643 98

Male New Zealand White rabbits were orally given 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily for 10 days and were treated with glutathione-precursors and depletor, antibacterial agents, or sodium thiosulfate. The drug administered, the mortality, and the mean survival time were as follows: corn-oil controls (0), euthanatized at 25 days; AFB1-controls (2), 21 days; AFB1 and saline controls (2), 22 days; cysteine and AFB1 (5), 13 days; methionine and AFB1 (5), 12 days; sodium thiosulfate and AFB1 (2), 21 days; sulfadimethoxine and AFB1 (1), 24 days; oxytetracycline and AFB1 (0), euthanatized at 25 days; and ethyl maleate and AFB1 (3), 21 days. Clinical signs of toxicosis included decreased feed consumption during AFB1 administration, loss of body weight or failure to gain, and death. Clinicopathologic changes included increases in serum bilirubin concentration and alanine aminotransferase and aspartate aminotransferase activities. Prothrombin and activated partial thromboplastin times were lengthened. Plasma fibrinogen concentration was decreased. Changes in PCV, hemoglobin concentration, and serum alkaline phosphatase were unremarkable. Oxytetracycline had protective effects against chronic aflatoxicosis in rabbits. Cysteine and methionine enhanced chronic aflatoxicosis.
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PMID:Effects of various treatments on induced chronic aflatoxicosis in rabbits. 680 40

The purpose of this experiment was to compare the toxic effects of aflatoxin B1 (AFB1) and warfarin in pigs and to determine whether these have an additive effect in these pigs fed dietary Cd. Cadmium was provided daily through the diets of 2 concentrations (0 or control, and 83 micrograms/g of diet) during the 40 days of the experiment. At the start of the 5th week, AFB1 and warfarin were given in 5 daily doses (each dose 0.2 mg/kg of body weight) and the effects were determined for 10 days (starting with the 1st treatment day). Aflatoxin B1 given to the pigs fed the control diet (0 Cd) was toxic, inducing significantly increased alkaline phosphatase, sorbitol dehydrogenase, and aspartate aminotransferase activities and the prothrombin time (PT) and activated partial thromboplastin time (APTT) and significantly decreased values in serum total protein, alpha-globulin, beta-globulin, gamma-globulin, and fibrinogen. There was no effect on blood urea nitrogen. The treatment with warfarin was more effective in producing earlier and significantly longer PT and APTT. In the pigs fed the diet with the added Cd, differences in activity of alkaline phosphatase, sorbitol dehydrogenase, aspartate aminotransferase values, but not blood urea nitrogen, as well as differences in intensity and duration of response in PT and APTT occurred when pigs were dosed daily for 5 days after AFB1 or warfarin. It is concluded that dietary Cd (83 micrograms/g of diet) in young pigs has an inhibitory effect on AFB1 toxicity and an enhancing synergistic effect with warfarin.
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PMID:Toxicology of aflatoxin B1, warfarin, and cadmium in young pigs: clinical chemistry and blood coagulation. 680 74

Thirteen biochemical parameters (viz. glucose, calcium, inorganic phosphorous, urea nitrogen, uric acid, cholesterol, albumin, total protein, total bilirubin, alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase) were determined in serum and partly in liver of rats 1-28 days after i.p. aflatoxin B1 (AFB) (3 mg/kg). Histological examinations of the liver were also made in parallel to the biochemical studies. In the serum, enzyme activities and total bilirubin level increased and peaked on the 2nd day, while other activities of aspartate aminotransferase and alanine aminotransferase in the liver significantly decreased and reached a minimum on the 2nd day after AFB administration. The depression of the liver enzyme activities persisted over 7 days. The liver protein content also reduced transiently during 1-1.5 days. However, all biochemical parameters returned to normal levels 2 weeks after treatment, and remained so throughout the rest of experimental period. Histological changes in the liver were very similar to those reported by other.
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PMID:Sequential biochemical and histological changes in rats treated with aflatoxin B1. 742 38

In order to evaluate the relative contribution of aflatoxin B1 (AFB1)-induced toxicity towards a methyl-deficient diet influenced AFB1 carcinogenesis, a no-observed-effect-level (NOEL) for AFB1, with reference to liver damage, was determined in rats fed a nutritionally complete amino acid-defined basal (CMS) diet or a choline-methionine-deficient (CMD) diet. After 3 weeks of dietary treatment, male Fischer 344 rats received a single, oral dose of AFB1 in the range of 100-600 pg/kg body weight. At 24, 48 and 72 h after AFB1 treatment, six serum biochemical parameters were analysed in parallel with histological examination of liver sections. In rats fed the CMS diet and receiving 250-600 micrograms/kg AFB1, serum levels of glutamyl oxalo-transaminase (SGOT), glutamyl pyruvic transaminase (SGPT), alkaline phosphatase (ALP) and total bilirubin increased, glucose levels decreased and gamma glutamyl transpeptidase (GGT) levels remained unchanged over the 72-h period following mycotoxin treatment. However, at 100 micrograms/kg AFB1, these serum parameters remained at control levels. Pathological examination of liver sections indicated no significant lesions at 100 micrograms/kg AFB1 confirming this as the non-necrogenic dose or NOEL in CMS diet group rats. In contrast, in CMD diet fed rats, serum or pathology data showed no obvious time- or dose-response to mycotoxin treatment, extensive hepatic lipidosis in response to dietary treatment being the only predominant lesion in this diet group. The milder response of CMD rat livers to a single dose of AFB1 suggest a possible reduction in the susceptibility of these livers to AFB1 toxicity.
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PMID:Acute hepatic response to aflatoxin B1 in rats fed a methyl-deficient, amino acid-defined diet. 809 59

Ninety-six crossbred weanling pigs (36 d of age, initial weight of 8.8 kg) were used in a three-phase study to determine the effects of feeding an aflatoxin-contaminated corn (AC) diet (922 ppb of aflatoxin B1) with and without sodium bentonite (clay) on performance, liver function, and mineral metabolism. In the nursery phase, control corn (NC) or AC was fed in corn-soybean meal diets with and without 1% clay for 6 wk. Compared with NC, AC decreased ADFI and ADG (P < .01) and increased serum activities of gamma-glutamyltransferase (P < .01) and alkaline phosphatase (P < .05). In the growing phase, 48 pigs from the nursery phase were fed NC but continued on their respective clay treatments for 5 wk. Pigs previously fed AC had higher (P < .01) ADFI and lower (P < .05) gain/feed, serum Ca, K, and glucose; ADG, other serum values, and liver minerals were not affected by treatments. In the metabolism phase, 24 barrows from the nursery phase were continued on the same corn and clay treatments for two 4-d total collections of urine and feces. Feeding AC increased (P < .05) P and Na absorption. The addition of clay lowered Mg and Na absorption (P < .01) for both AC and NC. Significant interactions for many minerals indicated that the effects on mineral metabolism were more pronounced when AC was fed. Serum and liver mineral concentrations were generally unaffected by the treatments in all phases. Feeding clay with AC results in partial restoration of performance and liver function without greatly influencing mineral metabolism.
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PMID:Effects of feeding aflatoxin-contaminated diets with and without clay to weanling and growing pigs on performance, liver function, and mineral metabolism. 809 47


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