[Desmofibrinogenic activity of transamidases and thiol groups in plasma and tissues after aflatoxin B poisoning].
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “Aflatoxin Poisoning”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Search for lesions caused by aflatoxin B1 poisoning in 3 industrial chicken farms on the Ivory Coast].
A systematic search for feed contamination by aflatoxin-B1 as well as for lesions indicating an acute or chronic aflatoxicosis was made in three groups of industrially raised hens in Côte-d'Ivoire. The contamination rates were low although they were 6 to 10 times higher than the official standards. No lesion due to an acute or chronic intoxication by aflatoxins was observed. However, the repeated intake of small amounts of aflatoxins might eventually have repercussions on the technics-economical performance either by a direct action of the toxin or via the development of an immune depression in the animals.
Aflatoxin B1↗
Major biological consequences of aflatoxicosis in animal production.
Aflatoxins, a family of closely related, biologically active mycotoxins, have been known as a prominent cause of animal disease for 30 yr. The toxins occur naturally on several key animal feeds, including corn, cottonseed, and peanuts. Occurrence of aflatoxin on some field crops tends to spike in years when drought and insect damage facilitate invasion by the causative organisms, Aspergillus flavus and A. parasiticus, which abound in the crop's environment. Acute aflatoxicosis causes a distinct overt clinical disease marked by hepatitis, icterus, hemorrhage, and death. More chronic aflatoxin poisoning produces very protean signs that may not be clinically obvious; reduced rate of gain in young animals is a sensitive clinical register of chronic aflatoxicosis. The immune system is also sensitive to aflatoxin, and suppression of cell-mediated immune responsiveness, reduced phagocytosis, and depressed complement and interferon production are produced. Acquired immunity from vaccination programs may be substantially suppressed in some disease models. In such cases the signs of disease observed are those of the infectious process rather than those of the aflatoxin that predisposed the animal to infection. Mixtures of aflatoxin with other mycotoxins can result in greatly augmented biological responses in terms of rate of gain, lethality, and immune reactivity. Because of its great biological activity, its wide-spread potential presence in areas where critical feed crops are grown, and its propensity to spike in problem years, aflatoxin promises to be a continuing problem in animal production.
Animal Feed↗
Perak, Malaysia, mass poisoning. Tale of the Nine Emperor Gods and rat tail noodles.
In October 1988, a series of food poisoning cases occurred in the State of Perak in Malaysia. Most of the victims were children. Ultimately 13 children between the ages of 2.5 and 11 years died. Epidemiological investigations showed that the probable source of the poison was Loh See Fun, a noodles in the shape of a rat's tail. All the deceased ate the noodles from one supplier. Clinical and pathological findings were similar in each case. Postmortem examination was performed in 11 cases. Toxicological examination on organs in 10 cases showed a high concentration of aflatoxin in tissues of the deceased. High levels of boric acid were excreted from most of the victims. Histological examination of the liver in these cases showed necrotic changes found in aflatoxin poisoning. Combination of the epidemiological, clinical, toxicological, and pathological findings pointed to the fact that there was a common toxin or toxins responsible for the deaths. These were thought to be a combination of boric acid and aflatoxin.
Boric Acids↗
Clinical implications of food contaminated by aflatoxins.
Aflatoxins have been incriminated, mainly on circumstantial evidence, in hepatocellular carcinoma, acute hepatic failure and Reye's syndrome, but other possible effects of continuous or intermittent dietary exposure to aflatoxins, which occurs widely in the tropics, have received little study. Over the past 10 years evidence has steadily accumulated that incriminates aflatoxins in the aetiology of kwashiorkor, a widespread and serious disorder of children in the tropics, previously believed to be caused by protein deficiency. Investigation of human breast milk, undertaken initially to elucidate the pathogenesis of kwashiorkor in breastfed infants, has revealed widespread and serious exposure to aflatoxins from this source. Extension of these studies to pregnant women, in turn, revealed widespread and serious prenatal aflatoxin exposure. In laboratory and farm animals, such exposure has serious implications for immune and hepatic functions, and is detrimental to growth and development. Recent analysis of heroin samples show that heroin addicts may also be exposed to these toxins. These findings show that human exposure to aflatoxins may begin prenatally, persist during breastfeeding, and continue into adult life. It is postulated that aflatoxins (i) play a role in the aetiology of kwashiorkor, (ii) increase neonatal susceptibility to infection and jaundice, (iii) increase childhood susceptibility to infections and malignant disease, (iv) compromise immune responses to prophylactic immunisations and (v) may play a role in the pathogenesis of diseases in heroin addicts. There are indications also that acute, fatal aflatoxin poisoning which masquerades as 'hepatitis' may occur more frequently than is currently appreciated.
Acute Disease↗
Aflatoxin-the deadly poison.
Explore the source record for details and available documents.
Aflatoxins↗
An outbreak of aflatoxicosis and boric acid poisoning in Malaysia: a clinicopathological study.
An outbreak of food poisoning resulting in 13 deaths in children occurred in Malaysia during the Chinese Festival of the Nine-Emperor Gods in 1988. The offending food was a Chinese noodle called 'Loh See Fun' (LSF). The source was traced to a factory where a banned food preservative was added to make the LSF. The food poisoning was attributable to aflatoxins and boric acid. The clinical features included vomiting, pyrexia, diarrhoea, abdominal pain, anorexia, giddiness, seizures, and eventual coma. Initially, many presented with a Reye-like syndrome. Eleven post-mortem examinations were performed. The pathological findings included extensive coagulative necrosis of the liver with proliferative 'ductal/ductular metaplasia of the hepatocytes'. Giant cell formation, central vein sclerosis, bile stasis, and steatosis were also noted. There was presence of acute tubular necrosis, superficial upper gastrointestinal erosions, and ensuing encephalopathy. The eventual cause of death is acute hepatic and renal failure.
Aflatoxins↗
[Excretion of aflatoxine in milk in experimental aflatoxicosis of dairy cows].
Explore the source record for details and available documents.
Aflatoxins↗
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↗
Laboratory diagnosis of chemical intoxications.
Explore the source record for details and available documents.
Animals↗
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↗
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↗
[Prevention of mycotoxicoses (review of the literature)].
Explore the source record for details and available documents.
Animals↗
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↗
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↗