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Results for “Aflatoxin Poisoning”

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At least 73 records · Page 4Linked to original sources
PubMed1975

Bright greenish-yellow fluorescence and aflatoxin in agricultural commodities.

The corn milling industry has widely accepted the presence of bright greenish-yellow fluorescence under a black light as a presumptive indicator of aflatoxin (a poison produced by the mold Aspergillus flavus). This test was applied to wheat, oats, barley, rice, coconut, white corn, yellow corn, peanuts, sorghum, and soybeans, and evaluated in the laboratory. Our study supported the use of bright greenish-yellow fluorescence as a presumptive test for aflatoxin in wheat, oats, barley, corn, and sorghum.

Aflatoxins↗
PubMed1976

[Mycotoxins as a cause of disease in human beings].

Secondary metabolites, toxic to macro-organisms and micro-organisms, are produced by certain molds and some plant parasitic living fungi. A risk is given for man worldwide by ingestion or apparently also be other routes always undetected. In vivo-effects of the various mycotoxins are different, but mainly the liver is affected, expecially by the intake of smaller amounts of these poisons. Accordingly cirrhosis of the liver or primary liver carcinoma are expected in man as well as in animals and were already proved outside of Europe.

Chemical and Drug Induced Liver Injury↗
PubMed1977

Diet and cancer.

Differences in food intake patterns are positively correlated with differences in the incidence of various cancers in world populations. It is postulated here that dietary factors play a vital role in the genesis of several major neoplasms, specifically gastric and colon carcinomas. In addition to the food consumed, such variables as total caloric intake, nutrtional excess or deficit, exposure to carcinogens and consumption of alcohol also increase the risk of cancer. Through recognition of these factors and subsequent long-term manipulation of diet, it should be possible to reduce cancer morbidity and mortality.

Alcohol Drinking↗
PubMed1985

Aflatoxin and aflatoxicosis: V. The kinetic behaviour of dietary aflatoxins in colostrum drawn from cows postpartum.

This work was conducted in order to study the kinetic behaviour of dietary aflatoxins in the colostrum of a pregnant cow exposed to contaminated feeds for a short period. In this study, two pregnant cows received a single dose of dietary aflatoxins in the form of rice powder contained 31.20 ppm aflatoxin B and 19.68 ppm aflatoxin G during the last stage of pregnancy, at about two weeks before parturition. Samples of colostrum were collected from dams and assayed for the presence of toxic metabolites as well as its conjugations by electrophoretic analysis. The results revealed that the intake of aflatoxins appeared in the colostrum postpartum as AFM1 and also AFB2a which is a non toxic metabolite. Moreover, it was found that the excreted metabolites including AFB2a were conjugated to the immunoglobulin protein fraction of the colostrum. The significance of the obtained results to the newborn calf are discussed.

Aflatoxins↗
PubMed1978

Mycotoxicoses of animals.

Mycotoxicoses are intoxications caused by ingestions of foodstuffs contaminated with mycotoxins, i.e. toxic secondary metabolites of microscopic filamentous fungi (moulds). By field observations and by experimental testing, toxins or toxic strains of more than 100 species of fungi have been encountered. However, causal associations have so far only been established for a small number of mycotoxicoses in farm animals, and the more important mycotoxicoses are aflatoxicosis, facial eczema, mycotoxic nephropathy, and estrogenic syndrome. A full assessment of the impact of mycotoxins on the health of farm animals can hardly be made at present, because the amount of surveillance data from mycotoxicoses is very limited, due mainly to inadequate diagnostic criteria. A new set of criteria for the diagnosis of mycotoxicosis is proposed, which has been successfully applied in the causative study of mycotoxic porcine nephropathy.

Animal Feed↗
PubMed1996

Reduced cytochrome P450 and increased heme oxygenase in liver during rabbit aflatoxicosis.

The administration of aflatoxin B1 (AFB1) in New Zealand rabbit for 5 days at a daily oral dose of 0.05 or 0.1 mg/kg decreased microsomal hepatic cytochrome P450 whereas a dose-dependent increase in the reduced microsomal 420 nm absorption occurred. The nature of such an absorption was then investigated. Either in vitro incubation of control microsomal proteins with AFB1 up to 800 microM and NADPH, or primary rabbit hepatocyte cultures exposure to AFB1 up to 30 microM for 24 to 72 h, failed to produce any 420 nm absorbing species, suggesting that the 420 nm absorption observed in vivo was due to an hemoprotein increase. Chemical reductions of microsomal proteins from AFB1-treated rabbits confirmed this hypothesis. Enzyme activity determinations revealed an increase in both microsomal heme oxygenase and NADPH-cytochrome c reductase activities in AFB1 treated rabbits, suggesting that the 420 nm absorption observed in vivo was related to a particular increase in heme oxygenase.

Animals↗