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Hypothesis: plant and fungal biocides, copper and Indian childhood liver disease.

Hepatic copper accumulation is characteristic of Indian childhood cirrhosis (ICC) but in experimental animals causes only modest liver damage. Plant and fungal biocidal agents may be hepatotoxic, may increase hepatic copper concentration, and may be secreted in milk of lactating animals. Crotalaria species, Parthenium hysterophorus and Aspergillus flavus are possible contaminants of animal feeds in rural India, and we hypothesise that their products may be synergistic with copper in causing ICC.

Animals↗

Enzyme-linked immunosorbent analysis for aflatoxin B1.

An enzyme-linked immunosorbent analysis (ELISA) permitted the detection of less than 10 pg of aflatoxin B1 per ml. The antitoxin was most specific for aflatoxins B1 and B2alpha, and least specific for aflatoxin G1.

Aflatoxins↗

[Mycotoxicoses].

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Animals↗

[Toxic and metabolic liver injury (author's transl)].

Water soluble exogenous compounds are commonly excreted by the kidneys, but most of the exogenous substances are lipid soluble and have therefore first to be metabolized in the liver to water soluble compounds. Depending upon the nature of the chemical compound, the metabolism in the liver leads either to detoxification or toxification. Alcohol belongs to the most important substances which may cause severe liver injury. Alterations of the liver due to hydrocarbons as well as carcinogens, mycotoxins and thorium dioxide are relatively rare. Compounds such as analgesic and antiarrhythmic drugs, antibiotics, oral antidiabetic agents, antihypertensive and antirheumatic agents, chemotherapeutic drugs, hormones, laxatives, psychotropic drugs, thyreostatic and antineoplastic agents may also cause liver injury. For establishing the diagnosis, a detailed past history is required especially with respect to alcohol and drug consumption as well as regarding occupational exposure towards toxic compounds. Although the determination of liver enzyme activities in the serum may give some indication for liver cell injury, the histological examination of the liver by needle biopsy is required for the diagnosis. The therapy consists of the exclusion of the toxic compound and, if possible, of an increased elimination of the ingested toxins.

Alcoholic Intoxication↗

Immunological and HPLC detection of aflatoxin adducts in human tissues after an acute poisoning incident in S.E. Asia.

Acid hydrolysed, purified DNA, extracted from formalin fixed human tissues from persons acutely exposed to aflatoxins during a poisoning incident, was found to inhibit antibody binding in a competitive aflatoxin inhibition ELISA both before and after immunoaffinity column purification. HPLC analysis of acid hydrolysates of the DNA revealed a peak with a retention time 3 min earlier than 8,9-dihydro-2-(N7-guanyl)-9-hydroxy AFB1 synthesized either by peracid activation or direct reaction of the 8,9-oxide with DNA. The major peak seen when DNA was extracted from formalin fixed tissues from rats treated with aflatoxin B1 was identical to that seen in the formalin fixed human tissues. Adduct levels ranged from 0 to 170 x 10(6) nucleotides depending on tissue type and individual examined.

Adolescent↗

[Disease and depression of productivity in raising swine caused by mycotoxins].

Mycotoxins are natural substances, which are poisonous for man and animals. Mycotoxicological investigations, carried out from 1982 to 1986, showed that aflatoxins (B1, B2, G1, G2), trichothecenes (T-2 toxin, HT-2 toxin, diacetoxyscirpenol, monoacetoxyscirpenol, neosolaniol and deoxynivalenol) ochratoxin A and zearalenone are to be expected in feedstuffs. Further, sclerotia of Claviceps purpurea were found in cereals repeatedly, which demonstrates that also ergot alkaloids can be found in feedstuffs. The determined toxin concentrations often do not suffice to produce the described "classic" clinical symptoms and pathological changes. On the contrary the continuous intake of small amounts leads to chronic intoxications which are characterized by loss of weight, insufficient gain in weight, fertility disorder or increased susceptibility for infectious diseases. As feedstuffs are mostly contaminated by different kinds of toxinogenic fungi and as fungal strains are frequently able to produce several mycotoxins simultaneously, it must be assumed that naturally occurring mycotoxicoses are not monocausal, but multitoxic diseases. Although we have improved analytical methods, naturally occurring mycotoxicoses still cannot always be cleared up completely.

Animal Feed↗

[Poisoning in swine].

For clinical interests it is advisable to subdivide cases of swine poisoning in such as caused by food, drugs and environmental poisonings. This division gives pointers to aetiologic connections and special measures necessary for the clearing of the processes. With food poisoning mycotoxicoses play an evermore important role, whereas poisonings by trace elements are on the decrease. Sodium chloride poisoning often results primarily from insufficient water supply. With environmental poisonings carbon monoxide and cyanamide intoxication are presented. Poisonings caused by drugs are mainly the result of an overdose, of segregation in food or of non-licensed drugs. A relatively unknown swine poisoning by a drug against coccidiosis--licensed for poultry--is described.

Animal Feed↗

Animals as monitors of environmental quality.

The various species of domesticated and wild animals can be excellent monitors of environmental quality. Although analyses of industrial air and water effluents and tests for toxicants in soils, plants, foods and feeds may provide some degree of predictability of environmental quality, the ultimate monitors are those organisms having metabolic activities that are comparable to man. If we closely observe animals that share our environment, like the coal miner's canary, they will alert us to unseen and perhaps devastating environmental hazards.

Animal Diseases↗

Of sick turkeys, kwashiorkor, malaria, perinatal mortality, heroin addicts and food poisoning: research on the influence of aflatoxins on child health in the tropics.

Similarities between the geographical and climatic prevalences of kwashiorkor and of exposure to dietary aflatoxins, and between the biochemical, metabolic and immunological derangements in kwashiorkor and those in animals exposed to aflatoxins, prompted investigation of the associations between kwashiorkor and aflatoxins. Studies in Africa in the 1980s indicated a role for these toxins in the pathogenesis of the disease. Paediatric cases of kwashiorkor are less prone to severe Plasmodium falciparum malaria than normal children. In mice infected with P. berghei, aflatoxin exposure inhibits parasite growth and ameliorates morbidity. Aflatoxins occur in < or = 40% of samples of breast milk from tropical Africa, usually as low concentrations of the relatively non-toxic derivatives of aflatoxin B1 (AFB1) but sometimes as high concentrations of the very toxic AFB1. This could explain kwashiorkor in breast-fed babies. Aflatoxin exposure occurs in > or = 30% of pregnancies in tropical Africa and the toxins are often in cord blood, sometimes at extremely high concentrations. Aflatoxins are now incriminated in neonatal jaundice and there is circumstantial evidence that they cause perinatal death and reduced birthweight. Aflatoxin-induced immunosuppresion may explain the aggressive behaviour of HIV infection in Africa. There are similarities between observations on HIV cases in Africa and those on heroin addicts in Europe, where 'street' heroin is frequently contaminated with aflatoxin. Aflatoxins were found in 20% of random urine samples from heroin addicts in the U.K. and the Netherlands. Aflatoxins have also been incriminated in episodes of food poisoning which have been associated with serious morbidity and mortality, particularly among young children.

Adolescent↗

Selenium effect on the growth of carcinogenic fungi and cytotoxic action of aflatoxin B1 on lymphocyte culture and on embryonal development of Xenopus laevis.

The authors report the results of investigations on the protective effect of selenium against teratogenic and cytotoxic action of aflatoxin B1 and the inhibitory action of this element on the growth of fungi producing carcinogenic aflatoxins. Sodium selenate inhibited the growth of cultures of such fungi belonging to the class Fungi imperfecti as Aspergillus flavus, Aspergillus fumigatus, Penicillium meleagrinum and Penicillium rougolosum. Added to cell cultures of lymphocytes sodium selenate inhibited the cytotoxic action of aflatoxin B1 evidenced by inhibition of PHA-stimulated blastic transformation of these cells and reduction in the number of mitoses. Sodium selenate added to the medium in the culture of Xenopus laevis larvae poisoned with aflatoxin B1 reduced significantly the early mortality of embryos and counteracted the teratogenic action of aflatoxin B1. This action was observed, however, only in early phase of morulation. The authors discuss the importance of their observations for the studies on the role of bioelements deficiency in the environment for induction of malignant transformation.

Aflatoxins↗

[Elimination of aflatoxin B1 by clays from contaminated substrates].

It has been proved that clays were able to absorb aflatoxin B1. The amount of adsorbed aflatoxin depended on the nature of clay. The adsorbing power of the clays was checked in relation to some environmental factors. From this study, it is claimed that clays are suitable for détoxification of liquid food-stuffs poisoned by aflatoxin.

Adsorption↗