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At least 289 records · Page 16Linked to original sources
PubMed1982

Effect of some enzyme inducers, fluids, and methionine-thiosulfate on induced acute aflatoxicosis in goats.

Groups of four 6- to 12-month-old male goats were injected intraruminally with a lethal dose (3 mg/kg of body weight) of aflatoxin B1 (AFB1). Drugs were administered parenterally before (pretreatment) or beginning 8 hours after goats were doses with AFB1. These drugs were phenobarbital (PB), phenylbutazone (PBZ), piperonyl butoxide (PRO), benzoflavones, water, and 5% glucose solution (D5W). Most groups given the drugs after AFB1 was administered also were given intraperitoneal injections of methionine-sodium thiosulfate (MET-TS) solution. Clinical signs of toxicosis, serum aspartate aminotransferase activities, serum bilirubin concentrations, duration of illness, mortality, and gross and microscopic pathologic findings taken together indicated that toxicosis was increased with MET-TS + PB therapy, PBZ pretreatment, PBZ therapy, benzoflavone pretreatment, benzoflavone therapy, MET-TS + benzoflavone therapy, and MET-tS + water therapy. Toxicosis was not altered appreciably by MET-TS + PBO therapy. Beneficial effects (less severe toxicosis) were produced by PB pretreatment; these effects were prolonged maintenance of strength, vigor, and appetite and (in 1 goat that recovered) absence of pathologic changes or serum bilirubin increase. Therapy with MET-TS + D5W (but not MET-TS alone) also lengthened maintenance of strength, vigor, and appetite, but did not prevent pathologic changes. The beneficial effect of MET-TS therapy reported in a previous study (AFB2 dosage of 4 mg/kg) was not observed with the 3 mg/kg lethal dose. In conclusion, therapy for acute aflatoxicosis with inducers of hepatic microsomal enzymes is ineffective (PBO) or contraindicated (PB, PBZ, benzoflavones). Therapy with D5W may be a useful adjunct to other therapeutic drugs, but multiple intraperitoneal injections of D5W may decrease survival time because of stress.

Aflatoxin B1↗
PubMed1982

Effect of enzyme inducers and inhibitors and glutathione precursor and depleter on induced acute aflatoxicosis in rabbits.

Male New Zealand White rabbits were treated with microsomal enzyme inducers, inhibitors of hemoprotein synthesis or action, and glutathione precursor and depletor before they were orally given the median lethal dose (LD50) of aflatoxin B1 (AFB1; 0.4 mg/kg) at the start of a 7-day experimental period. The drugs administered, mean duration of illness (hours), and survival percentage were as follows: controls (saline solution)-85, 50%; phenobarbital (PB)-100, 100%; phenylbutazone-115, 67%; benzoflavone-39, 17%; stanozolol-67, 67%; cobaltous chloride (CoCl2)-46, 67%; piperonyl butoxide (PBO)-88, 100% cysteine (CYS)-68, 100%; ethyl maleate-71, 83%. Signs of toxicosis included decreased feed and water consumption, weight loss, dehydration, lethargy, and emaciation; some rabbits died or were euthanatized. Clinico-pathologic changes included increased serum aspartate aminotransferase (AST) activity by 24 hours and bilirubin concentration by 48 to 72 hours after AFB1 was given. Grossly, livers were pale or tan and friable, with prominent lobular architecture. Kidneys of affected rabbits were pale to dark red. Microscopically, livers were normal or had lesions as great as extensive necrosis, hemorrhage, mineralization, and bile duct proliferation. Treatment of rabbits with PB, CoCl2, PBO, and CYS protected against AFB1 hepatic pathology, and PB, PBO, and CYS also had protective effect against lethality. Ethyl maleate provided some protection against lethality and increased serum AST activity and bilirubin concentration. Toxicosis was enhanced by benzoflavone; phenylbutazone and stanozolol had litte influence.

Acute Disease↗
PubMed1982

Toxicology of aflatoxin B1, warfarin, and cadmium in young pigs: performance and hematology.

Observations on the interactions of cadmium (Cd) x aflatoxin B1 (AFB1) and Cd x warfarin included several variables of animal performance and hematology. Cadmium was fed daily for 40 days (groups IV, V, VI) and a Cd-free diet was fed to groups I, II, and III. Groups II and V were treated with AFB1, and groups III and VI were treated with warfarin--each for 5 days during the 5th week of the experiment and the effects were observed for 10 days. All pigs fed the diet with added Cd had developed severe anemia by the 4th week of the experiment. The incorporation of this toxic concentration of Cd (83 micrograms/g) in the diet seemed to have blocked the liver microsomal enzyme system (cytochrome P-450), diminishing the toxic effects of 5 daily oral doses (0.2 mg/kg of body wt) of AFB1 (group V pigs), but enhancing synergistically the toxic anticoagulant effects of the same doses of warfarin in young pigs (group VI). The data presented also indicated that the feeding of toxic concentrations of Cd stimulated increased glutathione peroxidase activity, which conjugated the AFB1 epoxides with their excretion as reduced glutathione but enhanced the toxic anticoagulant effects of warfarin in young pigs.

Aflatoxin B1↗
PubMedDate not supplied

[Immune reactions in malnutrition and aflatoxin blastomogenesis].

Experiments were made on 80 male Wistar rats kept for 210 days on the common (respectively restricted protein) diet and exposed to aflatoxin intoxication. Humoral immunity was elucidated by qualitative and semi-quantitative immunoelectrophoretic analysis of the IgG and IgM levels, as was the presence of circulating autoantibodies in the test animals' serum. At the end of the experiments the development of leiomyosarcomas was noted in the absence of primary neoplastic transformation in the liver. The tumors were less incident in the animals kept on the low-grade diet than in those kept on the full-value diet. Immunoassay revealed the presence of humoral immunity inhibition under malnutrition. During protein deficiency there were no circulating autoantibodies against mesenchymal tissue antigens which were found in the serum of the animals fed ad libitum. It is assumed that immune deficiency in malnutrition is also accompanied by inhibition of the so-called enhancement phenomenon in the course of aflatoxin blastomogenesis. It is likely that the immunological mechanisms cited have an effect on the histogenesis as well as on the development of aflatoxin tumors.

Aflatoxin B1↗
PubMed1981

[Influence of one-time aflatoxin intoxication on lysosomes and ultrastructure of liver cells].

White male Wistar rats were treated with 6 and 10 mg/kg of Aflatoxin Bi intraperitoneally. 3 h afterwards, they were decapitated and their livers processed after the classical histological methods for electron microscopy as well as after the method of Gomory-Holt for acid phosphatase in liver tissue. The ultrastructural changes affected the nucleus and its chromatin; the rough and smooth endoplasmic reticulum were vacuolised; the Golgi apparatus was activated; the autophagic function of the hepatocyte lysosomes was underlined, as well as the heterophagic in the Kupffer cells. The findings are discussed as signs of early degenerative process, or of lipophanerosis.

Animals↗
PubMed1981

Chronic aflatoxicosis in cattle.

Pathological, hematological and plasma enzymatic studies were made on milk cattle affected by chronic aflatoxicosis caused by the prolonged feeding of concentrate feed mixtures containing contaminated groundnut cake having aflatoxin B1 (110 ug/kg groundnut cake at the time of sampling), B2, G1 and G2. Clinical and necropsy observations on liver included proliferation of connective tissue along portal triads leaving small group of hepatocytes intact. Liver function tests showed liver damage in three of the four affected animals studied.

Aflatoxins↗
PubMed1981

Experimental aflatoxicosis in swine: morphological and clinical pathological results.

The morphological changes in livers of 30 feeder pigs fed diets containing corn contaminated by aflatoxins (0.0 microgram aflatoxins/g feed, 0.4 microgram aflatoxin/g feed, and 0.8 microgram aflatoxin/g feed) were compared with changes in hematology, liver specific serum enzymes, serum proteins, and lymphocyte stimulation indices. Histologically, the livers were classified into five groups. Pigs fed the 0.8 microgram/g diets had the most severe histological lesions of karyomegaly, bile ductule proliferation and hepatocellular degeneration plus elevated gamma-glutamyl transpeptidase, aspartate aminotransferase, and alkaline phosphatase. This group also had significantly lower total protein and albumin values compared to the control pigs. Variation in the severity of the histological lesions was seen in pigs fed 0.4 microgram/g diets as well as variation in lymphocyte indices, liver specific serum enzymes, and electrophoretic results in the affected pigs in that group.

Aflatoxins↗
PubMed1980

Aflatoxicosis in swine: a review.

Chronic effects of aflatoxins may be reducing the efficiency of swine production unit by decreasing the immune response leading to increased susceptibility to disease and increased mortality, and decreasing resistance to stress. The individual pig's response to aflatoxin is affected by many factors, but age is especially important with the younger pig much more susceptible to damage than older pigs. The greatest problem with aflatoxins in the United States appears to be in the Southeast and is associated mostly with corn and cottonseed meal. Management factors are important in the prevention and reduction of aflatoxins in feed. A simple quantative test for aflatoxins has been developed for field surveys of suspected feed and a decontamination process has also been developed.

Animal Feed↗
PubMed1995

An outbreak of acute hepatic encephalopathy due to severe aflatoxicosis in Malaysia.

In October 1988, 13 Chinese children died of acute hepatic encephalopathy in the northwestern state of Perak in peninsular Malaysia. The acuteness of the illness differed from previously reported outbreaks described in Kenya, India, and Thailand. Epidemiologic investigations determined that the children had eaten a Chinese noodle, loh see fun, hours before they died. The attack rates among those who had eaten the noodles were significantly higher than those who had not (P < 0.0001). The cases were geographically scattered in six towns in two districts along the route of distribution of the noodle supplied by one factory in Kampar town. Aflatoxins were confirmed in postmortem samples from patients. This outbreak has important public health implications for many developing countries.

Acute Disease↗
PubMed1994

Serum hepatitis in two brood mares.

Two adult Quarter Horse mares from the same farm developed signs of hepatic disease approximately 2 months after parturition. Both mares had received tetanus antitoxin at the time of foaling. One mare developed subcutaneous edema of the distal aspect of all 4 limbs, photodermatitis involving unpigmented areas of skin, and high serum activities of liver-specific enzymes. The other mare had signs of acute hepatic failure, including icterus, hepatic encephalopathy, and high serum activities of liver-specific enzymes, and died. The second mare had signs typical of serum hepatitis (Theiler's disease) and the first mare was believed to have had an atypical, less-severe form of serum hepatitis. Hepatotoxic agents (eg, poisonous plants, aflatoxins, toxic chemicals) were not found on the farm.

Animals↗
PubMed1994

[Aflatoxicosis in Antwerp bearded bantams (Gallus gallus)].

Aflatoxicosis is a worldwide disease especially of poultry and swine. The toxin is found frequently in different kinds of nuts and cereals from tropical areas. In the present report the cause of disease in "Antwerpener Bartzwergen" after unsuccessful treatments could be correlated with Aflatoxine in the amounts of 1629, 759, 5 and 5 micrograms/kg resp. for Aflatoxin B1, Aflatoxin G1, Aflatoxin B2 and Aflatoxin G2 in the groundnuts.

Animal Feed↗