Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were given a single dose of aflatoxin B1 lethal to 50% of the animals (7.20 mg/kg). Their livers were examined histochemically in correlation with sequential histological lesions. Early periportal liver cell necrosis and marked biliary cell proliferation were observed. Periportal cytoplasmic glycogen and RNA depletion occurred during this early period and subsequently extended to the whole lobule. The enzymes investigated decreased or disappeared in the periportal area; but alkaline phosphatase increased strikingly in the centrolobular area, whereas canalicular adenosinetriphosphatase completely disappeared throughout the liver lobule. The histochemical changes reverted to normal after cessation of the necrosis. Histochemical techniques were more sensitive in detecting the vulnerability of the periportal parenchyma to aflatoxin. After the necrosis, regenerative foci appeared. They showed a variable content in glycogen and RNA and were characteristically enzyme deficient. This reflects the immaturity of regenerating hepatocytes. These early foci subsequently disappeared and are thus considered irrelevant to hepatomagenesis.
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PMID:Sequential histological and histochemical study of the rat liver after single-dose aflatoxin B1 intoxication. 12 26

Male Wistar rats were given 50 mug of aflatoxin B1 twice a week for 4 weeks, and thereafter 75 mug twice a week for 10 weeks. Their livers were investigated histologically and histochemically for glycogen, RNA, fat, alkaline and acid phosphatases, adenosine triphosphatase, 5'-nucleotidase, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, succinic dehydrogenase, and alkaline and acid nucleases. No significant lesions occurred before 15 weeks. During this period, the liver was histochemically unchanged except for a periportal decrease of alkaline phosphatase and adenosine triphosphatase. Scattered hepatocytes with a strong glucose-6-phosphatase activity appeared. These changes represent toxic effects of aflatoxin B1 and are irrelevant to carcinogenesis. From 15 weeks onward, three types of liver cell hyperplastic foci and nodules developed. Histologically, and with respect to glycogen, fat, and RNA content, only two of these types were considered as potential precursors of hepatocarcinomas. However, all types exhibited a decrease or absence of the enzymes studied. Both histological and histochemical changes stressed the complex heterogeneity existing between and within hepatic foci and nodules. From 11 months on, hepatocarcinomas developed. The tumors disclosed similar histochemical changes. This similarity further supports the "precarcinomatous" nature of hyperplastic foci and nodules. It appears that focal changes in surface as well as in cytoplasmic and nuclear enzymes are intimately and very early linked to the carcinogenic process. Whether they are fundamental or only represent an epiphenomenon remains unclear.
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PMID:Sequential histological and histochemical study of the rat liver during aflatoxin B1-induced carcinogenesis. 16 70

The effect of ip administrated aflatoxin B1 and rubratoxin B, singly and in combination, on dogs was determined by serum tests, by observations of clinical signs and survival times, and by evaluation of gross and microscopic lesions. The dog is sensitive to the toxic effects of both mycotoxins. Glutamic-oxaloacetic transaminase, lactic dehydrogenase and alkaline phosphatase activities and survival time varied in relation to dose and to the mycotoxin(s) administered. All three plasma enzymes were elevated regardless of dose with the combination of aflatoxin B1/rubratoxin B at 24 hr after dosing, except LDH, which was within the normal range but only at the lowest dose level. Several serum constituents including BUN, cholesterol, uric acid, and total bilirubin were elevated, whereas serum glucose was depressed in dogs treated with the multiple-toxin regimen; these changes were not seen in dogs given only aflatoxin B1 but were characteristic in rubratoxin-treated animals. In general, gross findings at necropsy were similar in all dogs regardless of the dose regimen. A striking similarity existed in the histologic changes observed between lesions experimentally induced by the mycotoxin combination and those lesions reported for dogs fed toxic feed in laboratory studies or in natural cases of hepatitis X. Of particular similarity were the severe kidney lesions observed in dogs exposed to the mycotoxin combination and kidney lesions reported in natural outbreaks of hepatitis X. There can be little doubt of an association between hepatitis X and aflatoxin B1, although it is apparent that the disease probably involves more than a single toxic factor. Our results suggest that hepatitis X in dogs includes aflatoxin B1 as a primary etiological factor but that rubratoxin B also may be involved.
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PMID:Acute toxicity of aflatoxin B1 and rubratoxin B in dogs. 58 96

This experiment was designed to compare 3 dose levels of aflatoxin B1 (0.0, 0.5, and 1.0 mg/kg of body weight) and 2 infection levels of Fasciola hepatica metacercariae (0 and 220) to determine whether an additive effect from aflatoxin B1 occurs when fascioliasis is present in dairy calves. Twenty-four male, Holstein calves, 4 weeks old, and averaging 45.8 kg each, were assigned at random to 6 treatment groups, 4 calves per group: group 1--negative control; group 2--0.5 mg of aflatoxin B1/kg; group 3--1.0 mg of aflatoxin B1/kg group 4--220 metacercariae; group 5--220 metacercariae plus 0.5 mg of aflatoxin B1/kg; and group 6-220 metacercariae plus 1.0 mg of aflatoxin B1/kg. The single oral dose of 220 metacercariae was given (groups 4, 5, and 6) at the start of the 10-week experiment, and 5 weeks later, the single oral dose of aflatoxin B1 was given (groups 2, 3, 5, 6). Results from the principals, as compared with that from the controls (group 1), included significant decreases of dry matter intake (P less than 0.006), body weight (P less than 0.024), and serum albumin (P less than 0.04), and in groups 4, 5, and 6 infected with 220 flukes, there were significantly increased values of prothrombin time (P less than 0.014), serum alkaline phosphatase (P less than 0.04), and serum sorbitol dehydrogenase (P less than 0.007). Significant differences in number of flukes recovered from liver were seen in groups 4 to 6 given 0, 0.5, and 1.0 mg of aflatoxin B1/kg (P less than 0.046). The single oral dose of 22* fluke metacercariae in groups 4, 5, and 6 resulted in significantly increased concentrations of serum total protein (P less than 0.003) and globulins (P less than 0.01). Results from the development of the flukes from metacercariae to the mature state with sizes, numbers, feeding habits, and pathologic lesions were described. Differences in numbers of flukes recovered from liver of groups 4 to 6 and the presence of pneumonia in calves of group 6 indicated aflatoxin B1 produced persisting, lowered resistance. In all animals necropsied, the liver was the organ most affected by aflatoxin B1 as well as with flukes. Periportal fibrosis, monocytic infiltration, fatty infiltration, and bile duct proliferation were the usual lesions induced by aflatoxin B1. Additive toxic effects were observed in the groups 5 and 6 dosed with flukes and aflatoxin B1, with significant variations of serum and plasma values, as well as increased severity of histopathologic changes.
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PMID:Toxic effects of aflatoxin B1 in male Holstein calves with prior infection by flukes (Fasciola hepatica). 85 Dec 69

At 20 degrees C, aflatoxin B1, at a sublethal dose, decreases the activity of alkaline phosphatase (EC 3.1.3.1), alpha-glucosidase (EC 3.2.1.20), esterase (EC 3.1.1.1), chymotrypsin (EC 3.4.21.1), leucine aminopeptidase (EC 3.4.11.1), and phosphoamidase (EC 3.9.1.1) biosynthesis in Bacillus thuringiensis (Berliner). In contrast, at 41 degrees C no significant decrease was observed. At this temperature, the mycotoxin is not destroyed or metabolized and bacterial cells are resistant to the toxin.
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PMID:[Effect of aflatoxin B1 on the enzymatic activities of Bacillus thuringiensis (Berliner)]. 88 28

Wistar albino female rats were maintained for 10 d on diets containing various levels of the vegetable Solanum nigrum. Simultaneously, they received daily intraperitoneal injections of aflatoxin B1 (AFB1) (either 0.2 or 0.4 mg/kg body-weight) diluted in propylene glycol. At the end of the experiment, all animals were killed and their serum and hepatic microsomes were prepared for assay of enzymes. Results showed that aminopyrine N-demethylase activity increased 2.5-fold with 200 (S200) and 600 (S600) g S. nigrum/kg diets. Activity of uridine diphosphate glucuronyltransferase (UDPGT) (EC 2.4.1.17) also increased twofold. Similar results were obtained with glutathione S-transferase (EC 2.5.1.18) activity which increased by 60% with diet S600. After AFB1 treatment, a general increase in the activities of the above enzymes was found, except for UDPGT in the group fed on diet S600. When rats were fed on the diet without S. nigrum, AFB1 induced an increase in alkaline phosphatase (ALP) (EC 3.1.3.1), aspartate aminotransferase (AST) (EC 2.6.1.1) and gamma-glutamyltransferase (gamma-GT) (EC 2.3.2.2) levels in the serum. AFB1 also induced increases in serum ALP and gamma-GT levels when rats were fed on diet S600.
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PMID:Effect of the leafy vegetable Solanum nigrum on the activities of some liver drug-metabolizing enzymes after aflatoxin B1 treatment in female rats. 190 29

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

Effects of aflatoxin B1 and T-2 toxin, administered daily within 7 days at the doses of 0.7 mg/kg and 0.54 mg/kg, respectively, on metabolism of Ca and on the vitamin D hormonal system were studied in young rats kept on a ration containing normal (0.025 mg/kg) and high (0.25 mg/kg) amounts of vitamin D. Administration of the mycotoxins caused hypocalcemia, a decrease in absorption of Ca as well as in activity of alkaline phosphatase in small intestine mucose, while alterations in spongy bones (of the type of osteopetrosis) were most distinct in T-2 toxin treatment. Concentration of 25(OH)D3 in blood serum and activity of 25-hydroxylase D3 in liver tissue were decreased by 28% and 58%, respectively, after administration of T-2 toxin, and by 34% nd 33%, respectively, after treatment with aflatoxin B1. In kidney activity of I-hydroxylase 25(OH)D3 was unaltered and the activity of 24-hydroxylase tended to decrease. After treatment with the mycotoxins content of nuclear receptors of 1,25(OH)2D3 was decreased in small intestine mucose, whereas cytoplasmic receptors were increased 2.5-fold, thus indicating the distinct decrease in the receptors internalization. High doses of vitamin D caused an increase of Ca content in blood serum and of its absorption in small intestine as well as normalized Ca content in cortical bone of rats treated with T-2 toxin. At the same time, activity of 1-hydroxylase 26(OH)D3 was increased in liver tissue, while concentration of 1,25(OH)2D3 receptors was reduced in small intestine, but internalization of the hormone receptors was maintained at low level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of mycotoxins aflatoxin B1 and T-2 toxin on the vitamin D3 metabolism and binding of its hormonal form 1,25-dihydroxyvitamin D3 in rats]. 284 63

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

A comparative slaughter feeding trial was conducted using crossbred Hereford-Angus steers. Cottonseed meal known to be contaminated with aflatoxins was fortified with long-grain rice cultures of Aspergillus flavus to produce complete rations that contained 0, 60, 300 and 600 ppb aflatoxin B1 (AFB1). Forty steers, weighing approximately 250 kg were randomly assigned to four equal treatment groups. Animals were housed in individual pens and fed the assigned contaminated ration ad libitum for 155 d. On d 156 all animals were placed on the control ration for 14 d. Animals were weighed and blood samples collected every month for clinical chemistry analysis. Liver, muscle and fat biopsies were collected at 6-wk intervals. These samples were stored in liquid N2 prior to analysis for aflatoxin M1 and B1 content. Separate liver samples were taken for histopathological examination. Aflatoxin was withdrawn from the diet 2 wk prior to slaughter. After 1 wk of withdrawal liver, muscle and fat samples were collected and assayed for AFB1 and aflatoxin M1 (AFM1). Liver samples also were taken for histopathological examination. Growth rates and feed intakes in the 60 and 300 ppb aflatoxin treatments were not significantly different from controls. The 600-ppb treatment group had a decrease in feed intake and rate of gain. Rations containing 60 and 300 ppb of aflatoxin had no significant influence on blood components and enzyme patterns. The 600-ppb treatment caused a slight, but consistent, increase in serum glutamic oxaloacetic transaminase and alkaline phosphatase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Feedlot performance and tissue residues of cattle consuming diets containing aflatoxins. 370 Feb 68


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