Toxic Effects Of Aflatoxin B1 Research Articles

Aflatoxin binders II: reduction of aflatoxin M1 in milk by sequestering agents of cows consuming aflatoxin in feed.

Sequestering agents bind dietary aflatoxin B1 (AFB1) and reduce absorption from an animal's gastrointestinal tract. As a result, they protect an animal from the toxic effects of AFB1 and reduce transfer of the metabolite, aflatoxin M1 (AFM1), into milk. Three experiments, using late-lactation Holstein cows fed AFB1-contaminated feed, were conducted to evaluate several potential sequestering agents for their abilities to prevent or reduce the transmission of AFM1 into milk. Six agents previously tested in our laboratory for AFB1 binding in vitro were evaluated in these experiments. These were: SA-20, an activated carbon (AC-A); Astra-Ben-20, a sodium bentonite (AB-20); MTB-100, an esterified glucomannan (MTB-100); Red Crown, a calcium bentonite (RC); Flow Guard, a sodium bentonite (FG); and Mycrosorb, a sodium bentonite (MS). Five of the six sequestering agents significantly (P < 0.01) reduced AFM1 contamination of milk (AB-20, 61%; FG, 65%; MS, 50%; MTB-100, 59%; and RC, 31%); whereas, AC-A, activated carbon, had no effect on AFM1 transmission at 0.25% of feed. By the first milking (1 day after cows consumed contaminated feed), AFM1 appeared in milk, then reached maximum levels after three days, and was absent from milk within four days after AFB1 was removed from the feed. Sodium bentonites at 1.2% of feed showed good potential as AFB1 binders; MTB-100, a yeast cell wall product, was equally effective at 0.05% in feed. Potential AFB1 binding agents should be evaluated experimentally to demonstrate efficacy. Our data show that sequestering agents can reduce AFM1 in milk of cows fed AFB1-contaminated feed.

Sequential pathology of experimental aflatoxicosis in quail and the effect of selenium supplementation in modifying the disease process.

Feeding of aflatoxin B1 @ 1 ppm to 2-week old Japanese quail for a period of 8 weeks produced gross and microscopic changes in the liver, skeletal muscles, heart and bursa of Fabricius. These included fatty changes, bile duct hyperplasia and lymphoid aggregation in liver; haemorrhages in thigh, breast muscles and myocardium; mild depletion of lymphocytes, cystic degeneration and fibrous tissue proliferation in bursa of Fabricius. More or less similar lesions were seen in quail chicks fed on aflatoxin with sodium selenite @ 5 ppm but these were of lesser intensity and appeared at later stages of the experiment thereby indicating that supplementation of selenium had some protective action against the toxic effect of aflatoxin B1 in Japanese quail.

Reduction of toxic effects of aflatoxin B1 by using baker yeast (Saccharomyces cerevisiae) in growing broiler chicks diets

This study was carried out to investigate the effects of adding baker yeast (BY), chlortetracycline (CTC) and both BY + CTC to a control diet containing 200 ng/g of aflatoxin B1 (C + AFB1) on performance, serum parameters and pathologyc alterations of broilers. A total 100 chicks (Ross PM 3) were divided into five groups in individual cages and each containing 20 animals. BY, a rich source of protein and vitamin B complex, was mixed into the diets at 2.0 %, CTC was mixed into the diet at 2.5 ng/g. Feed consumption, body weight and feed efficiency were recorded weekly. Serum parameters and pathologyc alterations were determined at the end of the study. Dead animals were recorded daily. Liver changes were clearly apparent in the C+AFB1and C+ AFB1+CTC most of the livers were enlarged, yellow and had pethecial hemorrhages. Canalicula cholestosis was absent in group C+AFB1 and C+ AFB1+CTC, but not others. When compared to the control (C) group, alkaline phosphatase (ALP), appear to be significantly increased in the C+AFB1 and C+CTC+ AFB1 groups. Serum glutamic oxalacetic transaminase (GOT)was increased in C+AFB1 birds. Serum alphaphetoprotein was not affected by the treatments. Feed consumption and body weight were significantly reduced in group AFB1. Birds receiving BY + AFB1, CTC + AFB1 and BY + CTC + AFB1 had a significantly higher body weight than group C+AFB1. Feed efficiency was better in group CTC + AFB1 than the others. The findings of this research suggest tha BY (2%) can partly counteract some of the toxic effects of AFB1.

Effects of Vitamin A Supplementary in the Feed to Reduce Toxic Effects of Aflatoxin B1 on Japanese Quails (Coturnix coturnix Japonica)

2 Abstract: A study was conducted to determine the efficacy of the antioxidant vitamin A, for reducing aflatoxicosis in Japanese quail (Coturnix coturnix Japonica) from hatch to 35 d of age. Sixty Japanese quail chicks were randomly divided into four groups, three treatments and one control. Control group was fed a basal diet while the treatment diets were supplemented with vitamin A (15,000 IU/kg feed), vitamin A (15,000 IU/kg) + low level of aflatoxin B (100 µg/kg) or aflatoxin B (100 µg/kg). The liver was swollen and a bright 1 1 yellow color; microscopically fatty metamorphosis, necrotic areas and infiltration of polymorphonuclears were observed in aflatoxin B group and was not seen in any other groups. Compared to control, aflatoxin B (AFB ) 1 1 1 reduced body weight gain (BWG) and feed conversion rate (FCR) by 9.3 and 7.6 % respectively. The addition of 15,000 IU/kg of vitamin A without aflatoxin B improved quail growth performance. Dietary vitamin A had 1 affect on BWG and feed consumption (P<0.05) and reduced the toxic effects of AFB , addition resulted less 1 toxicity in the liver and kidney than AFB group. FC was found significantly important during third and fourth 1 weeks in vitamin A and AFB added group (P<0.05) FCR was also better than AFB group. The concentration 1 1 of liver function enzymes serum glutamic pyruvic transaminase (GPT), serum glutamic-oxaloacetic transaminase (GOT), alkaline phosphatase (ALP) increased when AFB was added to the diet, whereas the 1 supplementation of the diet Vitamin A partially decreased this negative effects. These results demonstrate that vitamin A plays a complex role in the process of chemical aflatoxicosis and when added at 15.000 IU/kg in the diet can provide protection against the harmful effects of AFB for experimental period in Japanese 1 quail.

Toxic effects of aflatoxin B1 and ochratoxin A, alone and in combination, on chicken embryos

Toxic effects of aflatoxin B1 and ochratoxin A, alone and in combination, on chicken embryos

Effect of dietary protein level on aflatoxin B1 actions in the liver of weanling rats.

The hepatocarcinogenic responses of rats to aflatoxin B1 (AFB1) are believed to depend on microsomal activation of the toxin, followed by macromolecular binding. Dietary protein insufficiency is reported to reduce the level of microsomal metabolism, and therefore would be expected to reduce the AFB1-induced carcinogenicity. Indeed, diminished hepatocarcinogenicity in low-protein diet fed weanling rats that had received AFB1 has been reported. In the present study, carcinogenicity and other toxic effects of AFB1 (0.5 p.p.m.) fed to weanling male Fischer F344 rats on a low-protein diet (5%) or normal-protein (20%) diet for up to 8 weeks were examined. In our study, in contrast with the previous report, all animals that had survived some initial toxicity were found to have developed hepatic tumors or hyperplastic gamma-glutamyltransferase-positive foci a year later. The low-protein diet also produced sub-acute toxicity after AFB1 exposure in the weanling rats, leading to severe histological changes, and the death of about half the animals after 3-4 weeks of exposure. Animals fed an AFB1-containing normal-protein diet also exhibited AFB1-induced hepatocarcinogenicity, but not the sub-acute toxicity. The levels of hepatic enzymes involved in AFB1 metabolism were examined in animals fed the low- or normal-protein diets in the absence of AFB1. The low-protein diet, fed to 3 week weanlings for the subsequent 5 weeks, decreased hepatic cytochrome P450 levels, as well as the in vitro capacity of microsomal fractions to form AFB1-8,9-dihydrodiol, an index of AFB1-8,9-epoxide formation. Rats on a normal-protein diet did not show these changes. This discrepancy between the observed increase in sub-acute toxicity and decrease in microsomal activities in the low-protein fed animals implies that the toxic effects observed in these rats were not directly related to metabolic activation of the toxin. In contrast to the diminished microsomal in vitro AFB1 activation, however, in vivo AFB1-DNA adduct formation ability in rats receiving the low-protein diet in the absence of AFB1 was found to become elevated more rapidly during the 5 week experimental feeding period, compared with animals receiving the normal-protein diet. This was accompanied by a more rapid fall in the levels of AFB1-glutathione S-transferase isozyme activity in the low-protein fed animals. The results of this study on weanling rats support the importance of AFB1-GSH in protecting against the carcinogenic responses to AFB1, and probably also the sub-acute toxicity of the latter.(ABSTRACT TRUNCATED AT 400 WORDS)

An overview of aflatoxicosis of poultry: its characteristics, prevention and reduction.

Aflatoxicosis represents one of the serious diseases of poultry, livestock and other animals. The cause of this disease in poultry and other food-producing animals has been attributed to the ingestion of various feeds contaminated with A. flavus. This toxigenic fungus is known to produce a group of extremely toxic metabolites, of which aflatoxin B1 (AFB1) is most potent. Avian species especially chicks, goslings, ducklings and turkey poults are most susceptible to AFB1 toxicity. The toxic effects of AFB1 are mainly localized in liver as manifested by hepatic necrosis, bile duct proliferation, icterus and hemorrhage. Chronic toxicity in those birds is characterized by loss of weight, decline in feed efficiency, drop in egg production and increased susceptibility to infections. The incidence of hepatocellular tumors, particularly in ducklings, is considered to be one of the serious consequences of aflatoxicosis. Even though prevention and avoidance are the best way to control aflatoxicosis, natural contamination of crops with A. flavus is sometimes unavoidable. Such aflatoxin-contaminated feeds can be decontaminated using various methods which mainly focus on physical removal or chemical inactivation of the toxins in the feeds. Moreover, dietary additives such as activated charcoal, phenobarbital, cysteine, glutathione, betacarotene, fisetin and selenium have also been reported to be effective in the reduction of aflatoxicosis in poultry.

Quantitative Comparison of Formed in Rat and Mouse Covalent Aflatoxin-DNA Livers and Kidneys&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;

The covalent interactions between aflatoxin B1 (AFB1) and DNA were investigated in the inbred F344 rat and noninbred CD -1 Swiss mouse. A good correlation was found between the level of covalent modification of DNA, species sensitivity, and organ specificity, to the toxic effects of AFB1. The patterns of AFB1 acid hydrolysis products from DNA isolated from the livers and kidneys of both species were examined. The principal acid hydrolysis product in all cases was identified as 2,3-dihydro-3-hydroxy-(N7-guanyl)AFB1. Minor products consisted of adducts formed by the chemical transformation of the AFB1-N7-substituted guanine moiety forming putative formamidopyrimidine derivatives and the activation of AFB1 metabolites, which also modified the N-7 guanine atom. These last-mentioned products were present in greater amounts in resistant tissues. In vitro studies on the activation of AFB1 by microsomal fractions of mouse and rat livers found that mouse liver microsomes were rapidly inactivated.

Prevention by estradiol of aflatoxin-induced cytotoxicity in cultured chick embryo liver cells.

Aflatoxin B1 at a final concentration of 10(-5) M depressed the sytheses of DNA, RNA and protein in cultured chick embryo liver cells. The same dose produced ultrastructural changes in the nucleus, such as nucleolar compactness or segregation of fibrillar and granular components and in the cytoplasmic area, such as vesiculation, dilatation or degranulation of endoplasmic meticulum. These acute toxic effects of aflatoxin B1 were partially decreased by an addition of 4 X 10(-5) M estradiol-17 beta. Namely estradiol-17 beta significantly reduced the nucleolar compactness and segregation of fibrillo-granular components but did not improve the vesiculation, dilatation and degranulation of endoplasmic reticulum. Estradiol-17 beta also protected the liver cells from the aflatoxin B1-induced inhibition of nucleic acid and protein synthesis. These results suggest that the protective effect of estradiol-17 beta against the acute hepatotoxicity of aflatoxin B1 is mainly due to an antagonistic interaction of both compounds on the synthesis of nucleic acid in nucleolus.

Conditions for induction of bacteriophage from lysogenic Bacillus megaterium with aflatoxin B1.

The present study was conducted to determine whether or not aflatoxin B1 was an effective inducing agent for lysogenic bacteria and to characterize some of the parameters involved in induction. A lysogenic strain of Bacillus megaterium (NRRL-B-3695) and an indicator strain of this species (NRRL-B-3694) were used. Cultures of the lysogenic strain were incubated for various periods of time in the presence of aflatoxin B1. Plaque-forming units as well as colony-forming units were then determined. Results of the present study indicated that bacteriophage lysogenizing B. megaterium could be induced with aflatoxin B1. The optimum concentration for induction was 25 micrograms of toxin per ml of early-log-phase culture. Evidence suggested that: (i) higher concentrations of aflatoxin B1 formed hydrophobic complexes which would not efficiently induce B. megaterium; (ii) the toxic effect of aflatoxin B1 severely limited the number of cells which could be induced prior to killing action of the toxin; and (iii) concentrations less than 25 micrograms of aflatoxin B1 per ml were not efficient inducers of bacteriophage production nor did they demonstrate the toxic effect observed at higher concentrations.

Modification of hepatotoxic effects of aflatoxin B1 in rabbits by immunization.

Reduction of acute toxic effect of aflatoxin B1 was achieved by immunizing the rabbits with small amounts of bovine serum albumin-aflatoxin B1 conjugate. Rabbits after immunization showed lower mortality, near normal serum isocitric dehydrogenase activity, no abnormality in livers when challenged with a single dose of aflatoxin B1. The results suggest that immunization might be used prophylactically against aflatoxicosis.