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PubMed1968

Mycotoxins.

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Aflatoxins↗
PubMed2006

Changes in hepatic cytosolic glutathione S-transferase activity and expression of its class-P during prenatal and postnatal period in rats treated with aflatoxin B1.

The effect of aflatoxin B1 (AFB1) on the expression of glutathione S-transferase-P (GST-P) which is the major isoform of GST in developmental stages has been investigated in rat liver during prenatal and postnatal stages. Following administration of AFB1 (0, 0.5, 1.0, 2.0, 3.0 or 4.0 mg/kg bw) injected I.P on day 8.5 of gestation the number of dead or reabsorbed fetuses and malformed embryos were recorded. Then the fetal livers were processed for measurement of total GST and GST-P activities, using 1-chloro-2,4-dinitrobenzene (CDNB) and ethacrynic acid (ETA) as substrates respectively. RT-PCR using rat GST-P specific primers was performed on mRNA extracted from livers. Besides, the effects of AFB1 on hepatic GST and GST-P were assessed in groups of suckling rats directly injected with the toxin. The results show that a single dose of AFB1 (1.0 or 2.0 mg/kg bw) caused approximately 50-60% depletion in fetal liver GST towards CDNB. Postnatal experiments revealed that liver GST (using CDNB as substrate) was significantly induced (approximately 40%) in suckling rats injected with a single dose of AFB1 (3.0 mg AFB1/kg) 24 h before killing. Liver GST-P expression was unaffected due to AFB1 exposures of rats before and after the birth. This finding was substantiated by western blotting and RT-PCR techniques. These data suggest that AFB1-related induction in rat liver total GST after birth may be implicated in protective mechanisms against AFB1. In contrast, inhibition of this enzyme in fetal liver following placental transfer of the carcinogen may explain high susceptibility of fetal cells to trans-plancental aflatoxins. Furthermore, lack of influence of AFB1 on GST-P expression in developmental stages can role out the involvement of this class of GST in AFB1 biotransformation.

Aflatoxin B1↗
PubMed2006

Antigenotoxic effect of Saccharomyces cerevisiae on the damage produced in mice fed with aflatoxin B(1) contaminated corn.

The potential of Saccharomyces cerevisiae (Sc) was evaluated for reducing the micronucleated normochromatic erythrocytes (MNNE) rate in mice fed AFB(1) contaminated corn. The study included two groups fed AFB(1) contaminated corn (0.4 and 0.8 mg/kg), a control fed uncontaminated corn, another group fed uncontaminated corn and 0.3% of Sc (1 x 10(8) live cells/g), and two groups fed AFB(1) contaminated corn (0.4 and 0.8 mg/kg) plus 0.3% Sc. Weight and MNNE were determined weekly for six weeks. Subsequently, the same determinations were made for another three-week period, but in mice receiving only a normal diet, without AFB(1) and Sc. Results in the first period revealed the following: control and Sc fed mice had similar constant weight increase, and low MNNE rate; mice fed only AFB(1) showed weight decrease and significant MNNE increase; finally, Sc improved weight gain and reduced MNNE produced by AFB(1). In the second period, results exhibited a tendency similar to that of the previous phase in the control and Sc fed mice; the weight and MNNE values improved in the other groups. We also determined the capacity of Sc for adsorbing and modifying the mycotoxin structure. The mixture was filtered to obtain two phases, and AFB(1) content was measured. Sc revealed a potent adsorbent capacity; however, chromatographic determination suggested no structural modification.

Adsorption↗
PubMed1992

Selenium in the treatment of heavy metal poisoning and chemical carcinogenesis.

Selenium (Se) has been shown to counteract the toxicity of heavy metals such as cadmium, inorganic mercury, methylmercury, thallium and to a limited extent silver. Although not as effective as Se, vitamin E significantly alters methylmercury toxicity and is more effective than Se against silver toxicity. Vitamin E is very effective against lead toxicity but Se has little effect. The presumed protective effect of Se against cadmium and mercury toxicity is through the diversion in their binding from low molecular weight proteins to higher molecular weight ones. Se appears effective in counteracting the chemical carcinogens (3-methyl-4-dimethyl-aminoazobenzene, 2-acetylaminofluorene, diethylnitrosamine, aflatoxin, 7,12-dimethylben (a) anthracene, benzopyrene and 3-methylcholanthrene) used to induce skin, liver and mammary tumors, but much less effective against those (dimethylhydrazine, azoxymethane, methylazoxymethanol, bis (2-oxopropyl) nitrosamine, benzopyrene, 1 methyl-1-nitrosourea and n-methyl-n-nitro-nitrosoguanidine) used to produce tumors in the colon, lungs, trachea and pancreas in laboratory animals. In contrast, Se many even increase pancreatic carcinomas in animals treated with bis (2-oxopropyl) nitrosamine. The health implications in humans of Se and heavy metal toxicities and in cancer are discussed.

Animals↗
PubMed2006

Liver lesions produced by aflatoxins in Rana catesbeiana (bullfrog).

This study describes alterations induced in Rana catesbeiana (bullfrog) liver after extended dietary exposure to aflatoxins (AFs). Bullfrogs of both sexes were fed for 120 days a commercial chow blended with a rice bran-based mixture of AFs containing 667.0, 11.65, 141.74, and 3.53 mg/kg of AFs B1, B2, G1, and G2, respectively. Animals were sacrificed on study days 45, 90, and 120. Severe and progressive liver lesions with structural collapse, increased hepatocyte and biliary duct cell proliferation, appearance of basophilic hepatocytes, and diffuse scarring, were observed at all time points. There were no quantitative alterations in the liver melanomacrophage centers of the AFs-exposed animals. Increased amounts of lipid hydroperoxides, indicative of ongoing oxidative stress, were more evident in the Addutor magnum muscle than in the AFs-damaged livers. No tumors were found in the R. catesbeiana livers after 120 days of exposure to relatively high doses of AFs.

Aflatoxins↗
PubMed1987

Effects of pre-treatment with aflatoxin on a second aflatoxin treatment in guinea pigs.

Two-hundred guinea pigs, weighing approximately 500 grams each, were placed in 8 groups, 4 of which received 20 micrograms/kg/day of partially purified aflatoxin for 7 days, followed by a 7 day recovery period. Paired groups then received 0, 20, 35 or 50 micrograms/kg/day of partially purified aflatoxin for 21 days. Animals were sacrificed periodically from all groups and blood was drawn for chemical and immunologic analysis. Weight gains were recorded and histopathologic studies were done on all animals. Pretreatment did not protect guinea pigs from a second exposure, and in fact enhanced mortality and liver toxicity as determined by histopathology. Serum chemistries and immunologic parameters of guinea pigs dosed twice were less conclusive, as neither high nor low doses differed from guinea pigs treated once. Glycocholic acid concentrations were more sensitive than traditional enzymes (aspartate and alanine amino transferase, alkaline phosphatase) for indicating hepatotoxicity.

Aflatoxins↗
PubMed2005

Threat assessment of mycotoxins as weapons: molecular mechanisms of acute toxicity.

Mycotoxins are impractical as tactical weapons, butthey can be used by small poor terrorist organizations to poison food and water sources or can be released in crowded, confined areas. Crude concentrated or dried extracts of readily grown fungal cultures can be used as weapons. The production of fungal weapons does not require elaborate facilities for the growth of fungi, sophisticated equipment for the purification of the toxins, or highly trained personnel. Aflatoxin B1, fumonisin B1, ochratoxin A, and the trichothecenes T-2 toxin and deoxynivalenol could be weaponized for bioterrorism. Knowledge of the symptoms of intoxication and the biochemical mechanisms of action of mycotoxins is necessary for the rapid identification of the toxins, the development of prophylactic antidotes, and the design of effective treatments of affected persons. All of these mycotoxins except deoxynivalenol are carcinogens (Stark, A. A., Annu. Rev. Microbiol. 34:235-262, 1980; Stark, A. A., p. 435-445, in P. S. Steyn and R. Vleggaar, ed., Mycotoxins and phycotoxins, 1986; Stark, A. A., p. 47-60, in C. L. Wilson and S. Droby, ed., Microbial food contamination, 2000; Stark, A. A., and N. Paster, p. 60-64, in M. L. Wahlqvist, A. S. Truswell, R. Smith, and P. L. Nestel, ed., Nutrition in a sustainable environment, 1994). Because immediate and widespread death, illness, or panic is the goal of bioterrorists, the mechanisms by which mycotoxins exert acute toxicity are the focus of this article.

Aflatoxins↗
PubMed2001

Mycotoxins.

Horses consume feed grains and forages that can produce a range of mycotoxins resulting from mold invasion. Toxicosis of horses often occurs from fumonisins or aflatoxin in grains, from the tremorgenic mycotoxins in dallis grass, or from slaframine in red clover. Fumonisin toxicosis often is severe and fatal, and aflatoxin can be acute or chronic and debilitating. Other mycotoxins reported in horses may cause moderate to mild signs that regress when the contaminated feedstuff is removed. Overall, horses appear to have a relatively low prevalence of reported mycotoxicoses among domestic animals, but they are extremely sensitive to the fumonisins. Since there are no good therapies for mycotoxin poisoning, attention to providing high quality grains and forages to prevent mycotoxicoses is the most effective means for reducing the risk of mycotoxins in horses.

Animal Feed↗
PubMed2006

Hepatitis B virus x gene and cyanobacterial toxins promote aflatoxin B1-induced hepatotumorigenesis in mice.

AIM: To assess the combinative role of aflatoxin B1(AFB1), cyanobacterial toxins (cyanotoxins), and hepatitis B virus (HBV) x gene in hepatotumorigenicity. METHODS: One-week-old animals carrying HBV x gene and their wild-type littermates were intraperitoneally (ip) injected with either single-dose AFB1 [6 mg/kg body weight (bw)], repeated-dose cyanotoxins (microcystin-LR or nodularin, 10 microg/kg bw once a week for 15 wk), DMSO (vehicle control) alone, or AFB1 followed by cyanotoxins a week later, and were sacrificed at 24 and 52 wk post-treatment. RESULTS: AFB1 induced liver tumors in 13 of 29 (44.8%) transgenic mice at 52 wk post-treatment, significantly more frequent than in wild-type mice (13.3%). This significant difference was not shown in the 24-wk study. Compared with AFB1 exposure alone, MC-LR and nodularin yielded approximately 3-fold and 6-fold increases in the incidence of AFB(1)-induced liver tumors in wild-type animals at 24 wk, respectively. HBV x gene did not further elevate the risk associated with co-exposure to AFB1 and cyanotoxins. With the exception of an MC-LR-dosed wild-type mouse, no liver tumor was observed in mice treated with cyanotoxins alone at 24 wk. Neither DMSO-treated transgenic mice nor their wild-type littermates had pathologic alterations relevant to hepatotumorigenesis in even up to 52 wk. CONCLUSION: HBV x gene and nodularin promote the development of AFB(1)-induced liver tumors. Co-exposure to AFB1 and MC-LR tends to elevate the risk of liver tumors at 24 wk relative to exposure to one of them. The combinative effect of AFB1, cyanotoxins and HBVx on hepatotumorigenesis is weak at 24 wk.

Aflatoxin B1↗
PubMed1997

Urinary taurine as a non-invasive marker of aflatoxin B1-induced hepatotoxicity: success and failure.

The usefulness of urinary taurine as a non-invasive measure of hepatotoxicity of aflatoxin B1 (AFB1) was evaluated: changes in urinary taurine were characterized in a dose-response, acute toxicity experiment and in two sub-chronic, low dose exposure experiments. Urine of young, male, F344 rats was collected for 4 days prior to, and for 3 days after, the treatment with AFB1. Rats received a single p.o. dose of 0, 0.25, 0.5, 1, 2 or 3 mg AFB1/kg body wt. A transient increase in urinary taurine was noted with doses of 1, 2 or 3 mg AFB1/kg. In two sub-chronic exposure experiments, rats were gavaged with 25 microg AFB1/day for 5 successive days per week for 1 or 2 weeks (approximately 0.25 mg/kg/day). In the first experiment, only a transient increase in urinary taurine during 5 successive doses of AFB1 was observed, while in the second experiment, urinary taurine rose continuously during the 2 weeks of the AFB1 treatment. An explanation for these differing results is not obvious. Urinary taurine appeared to be a useful, non-invasive marker when hepatotoxicity was extensive. Unfortunately, at the low doses of AFB1 (0.25-0.5 mg/kg) as used in carcinogenesis experiments (10 doses of 25 microg/rat), urinary taurine appeared to be an insensitive measure of hepatic damage.

Administration, Oral↗
PubMedDate not supplied

Surveillance programmes for managing risks from naturally occurring toxicants.

Aflatoxins are potent carcinogenic, mutagenic and teratogenic metabolites produced by moulds that grow on food and feed. Their toxicity has caused severe health and economic problems worldwide. Other mycotoxins which have been associated with human health risks include ergot alkaloids, citreoviridin, trichothecenes, ochratoxins, citrinin, tremorgenic mycotoxins and the fumonisins. Many phycotoxins have also been associated with human illnesses; these phycotoxins include paralytic shellfish poisons, diarrhoeic shellfish poisons, ciguatera-related toxins, neurotoxic shellfish poisons, tetrodotoxin and, the more recently discovered, domoic acid which is associated with amnesic shellfish poisoning. Human exposure to these naturally occurring toxins can be from direct consumption of contaminated commodities or from foods derived from animals previously exposed to these toxins in their feed. Food safety monitoring programmes for selected toxins have been established for raw and finished products susceptible to contamination. Components of these control programme include the establishment of regulatory limits or guidelines, monitoring susceptible products for specific compounds, and the diversion of the contaminated products to lower-risk uses and/or decontamination procedures.

Consumer Product Safety↗
PubMed1989

Effect of a high affinity aluminosilicate sorbent on prevention of aflatoxicosis in growing pigs.

Adding 0.5% hydrated sodium calcium aluminosilicate to diets formulated with aflatoxin-contaminated corn significantly reduced the detrimental effects of the mycotoxin on live weight gains and feed intake. Hepatocellular changes normally associated with aflatoxin consumption could not be detected histopathologically in liver sections from pigs fed contaminated diets plus the aluminosilicate sorbent.

Aluminum Silicates↗