Ultrastructural changes were induced in rat liver by the single administration of aflatoxin B1 and G1. These were assessed at intervals of 1, 6, 18, 24 and 48 hours and 1, 4 and 8 weeks. It would appear that administration of aflatoxin B1 induced a marked nucleolar alteration seen from 6 hours after the injection. No significant alterations were noted in animals treated with a small amount of aflatoxin G1, but injection of a larger amount of aflatoxin G1 induced nucleolar alterations similar to aflatoxin Bl treatment. The nucleolar change was characterized by segregation of the granular and fibrillar elements. All three groups showed cytoplasmic changes, such as dilation of rough endoplasmic reticulum with detachment of ribosomes, hyperplasia of smooth endoplasmic reticulum, increased numbers of lipid droplets and microbodies. Autoradiographic studies have shown the absorbtion of both aflatoxin B1 and G1 in parenchymal cells, but aflatoxin Bl was absorbed more intensely than Gl, especially in the nucleus. Autoradiographic findings in electron microscopy showed a marked difference in the size grains between aflatoxin B1 and G1, aflatoxin G1 being 1arger than aflatoxin B1.
Aflatoxins/toxicity* ; Animal ; Autoradiography ; Comparative Study ; Liver/drug effects ; Liver/pathology* ; Male ; Microscopy, Electron ; Rats

Ultrastructural changes were induced in rat liver by the single administration of aflatoxin B1 and G1. These were assessed at intervals of 1, 6, 18, 24 and 48 hours and 1, 4 and 8 weeks. It would appear that administration of aflatoxin B1 induced a marked nucleolar alteration seen from 6 hours after the injection. No significant alterations were noted in animals treated with a small amount of aflatoxin G1, but injection of a larger amount of aflatoxin G1 induced nucleolar alterations similar to aflatoxin Bl treatment. The nucleolar change was characterized by segregation of the granular and fibrillar elements. All three groups showed cytoplasmic changes, such as dilation of rough endoplasmic reticulum with detachment of ribosomes, hyperplasia of smooth endoplasmic reticulum, increased numbers of lipid droplets and microbodies. Autoradiographic studies have shown the absorbtion of both aflatoxin B1 and G1 in parenchymal cells, but aflatoxin Bl was absorbed more intensely than Gl, especially in the nucleus. Autoradiographic findings in electron microscopy showed a marked difference in the size grains between aflatoxin B1 and G1, aflatoxin G1 being 1arger than aflatoxin B1.
Aflatoxins/toxicity* ; Animal ; Autoradiography ; Comparative Study ; Liver/drug effects ; Liver/pathology* ; Male ; Microscopy, Electron ; Rats

OBJECTIVETo evaluate the risk of liver cancer attributed to dietary aflatoxins exposure in Chinese residents.

METHODSMathematics model and "Margin of Exposure (MOE)" methods were employed in this study. The data used in mathematics model came from Joint FAO/WHO Expert Committee on Food Additives (JECFA) and the detection results of hepatitis B virus ( HBV) indicator in Chinese residents' blood sample in 2004. The data used in MOE model came from animal experiments, the fourth nutrition and health investigation among Chinese residents, and national inspection network for food contaminations.

RESULTSMathematics model indicated that for those people who were exposed to aflatoxins at average level (665.43 ng/d), the liver cancer incidence rate resulting from aflatoxins exposure was 0.4033 per 100 thousand person years. For those people who were exposed to aflatoxins at a high level (97.5 percentile, 24 787.20 ng/d) the liver cancer incidence rate attributed to aflatoxins exposure was 15.0215 per 100 thousand person years. Results from the MOE method showed that for the people in whole country, urban and rural areas who were exposed to aflatoxins at average level (0.011 09, 0.008 13 and 0.012 49 microg x kg(-1) x d(-1) respectively), the MOE values for aflatoxins to cause liver cancer were 9017.1, 12 304.7 and 8006.4 respectively. For those people who were exposed to aflatoxins at a high level (97.5 percentile, 0.413 10, 0.289 30 and 0.489 50 microg x kg(-1) x d(-1) respectively), the MOE values for aflatoxins to cause liver cancer were 242.1, 345.7 and 204.3 for whole country, urban and rural areas, respectively.

CONCLUSIONFor the people whose dietary aflatoxins exposure at average level, the risk of liver cancer attributed to aflatoxins is middle. For the people whose dietary aflatoxins exposure at high level, this kind of risk should be high.

Aflatoxins ; toxicity ; China ; epidemiology ; Diet ; Environmental Exposure ; Humans ; Liver Neoplasms ; epidemiology ; etiology ; Models, Theoretical ; Risk Factors

The mould phenomenon occurred commonly in the cultivation, processing and storage period of medicinal materials, which may result in production of mycotoxins. Mycotoxin contaminations caused by fungi are major issues related to the quality and safety of Chinese herbal medicine. This review summarized the work published in aflatoxins contamination of Chinese herbal medicine in China through the previous decade. The conclusion to be drawn from this survey is that aflatoxin exposure remains an important aspect of Chinese herbal medicine safety which needs to be paid great attention. We raised some points that should be focused on in future. The strategies of changing environment to suppress growth of toxin-producing fungus, so as to reduce aflatoxins are the most practical and effective ways, while biological control in the field production is a promising approach.
Aflatoxins ; analysis ; toxicity ; Animals ; China ; Cricetinae ; Cricetulus ; Drug Contamination ; prevention & control ; Fungi ; chemistry ; Herbal Medicine ; ethics ; Mycotoxins ; analysis ; toxicity

OBJECTIVEAflatoxin G1 (AFG1) is a member of the carcinogenic aflatoxin family produced by aspergillus flavus. It is a major contaminating mycotoxin in food in areas of China with high cancer incidence. The purpose of this study is to explore the carcinogenic effects of AFG1 in NIH mice.

METHODSNIH mice were randomly divided into three groups. Two experimental groups were treated intragastrically by gavage with AFG1 3 microg/kg and AFG1 30 microg/kg respectively, 3 times a week for 24 weeks. The control group was treated with normal saline. All mice were fed with food that was free of AFGs as confirmed by HPLC analysis. The mice were weighed every week throughout the entire experiment, and then sacrificed and examined pathologically at the 58th and 74th weeks respectively.

RESULTSCompared with control mice receiving no AFG1, bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were observed in mice receiving AFG1 treatment. The incidences of bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were 60.0%, 10.0% and 30.0% for mice receiving 3 microg/kg AFG1 and 28.6%, 35.7%, 42.9% for mice receiving 30 microg/kg of the toxin, respectively.

CONCLUSIONOral administration of AFG1 can induce hyperplastic lesions and adenocarcinoma of lung in NIH mice.

Adenocarcinoma ; chemically induced ; pathology ; Aflatoxins ; toxicity ; Animals ; Aspergillus flavus ; Carcinogens ; toxicity ; Lung Neoplasms ; chemically induced ; pathology ; Mice ; Random Allocation

ln order to investigate the mutagenic activity of Meju, an important component of the Korean diet, both chemical techniques and the Ames test were used. To determine if antimutagenic activity is present in Meju and other soybean based foods, the Ames Test was done in the presence of aflatoxin B1, benzo(a)pyrene, and other mutagens. Although aflatoxin contamination was found in 6 of 43 samples of Meju tested, the amounts were less than 1 ppb in all but one. Meju had a protective effect against mutations produced by both aflatoxins and benzo(a)pyrene, both of which act via an epoxide, but not against other mutagens tested.
Aflatoxins/analysis/*toxicity ; Fermentation ; Food Contamination/*analysis ; In Vitro ; Korea ; Mutagenicity Tests ; *Mutation ; Plant Extracts/toxicity ; Soybeans/*toxicity ; Support, Non-U.S. Gov't

To investigate toxicity of aflatoxin Gl and its mechanism, light microscopic, histochemical, electron microscopic and autoradiographic studies were done on the rat liver at various time intervals after the administration of aflatoxin Gl. Light microscopic alteration was first observed at 6 hours and necrosis of periportal hepatic cells was found at 18 hours. However, reduction of Feulgen positivity of the nucleus and pyroninophilia of cytoplasm was observed as early as 1 hour. Ultrastructural changes were noted at 6 hours and were advanced at l8 hours. Early changes consisted of nucleolar segregation, dilatation of rough endoplasmic reticulum, swelling of mitochondria and detachment of membrane bound ribosomes followed later by disruption of cytoplasmic organellae and focal necrosis. These changes were most marked at periportal region. Autoradiographic studies showed inhibition of H3-uridine incorporation into the nucleus at 1 hour, was most marked at 6 hours, and showed some recovery at 18 hours. H3-uridine labeling in the cytoplasm was also inhibited and the most marked inhibition was noted at 1 hour after the aflatoxin administration. These data indicate aflatoxin Gi has a hepatotoxic effect, particulary at the periportal region. This toxic effect is likely due to inhibition of nuclear RNA synthesis which leads to inhibition of ribosomal RNA and eventually protein synthesis. The DNA synthesis is also inhibited, as shown by reduction of Feulgen reaction in the nucleus.
Aflatoxins/toxicity* ; Animal ; Autoradiography ; Cell Nucleus/ultrastructure ; Cytoplasm/ultrastructure ; Histocytochemistry ; Liver/ultrastructure* ; Microscopy, Electron ; Mitochondria, Liver/drug effects ; Rats ; Uridine/metabolism

Aflatoxins produced primarily by two closely related fungi, Aspergillus flavus and Aspergillus parasiticus, are mutagenic and carcinogenic in animals and humans. Of many approaches investigated to manage aflatoxin contamination, biological control method has shown great promise. Numerous organisms, including bacteria, yeasts and nontoxigenic fungal strains of A. flavus and A. parasiticus, have been tested for their ability in controlling aflatoxin contamination. Great successes in reducing aflatoxin contamination have been achieved by application of nontoxigenic strains of A. flavus and A. parasiticus in fields of cotton, peanut, maize and pistachio. The nontoxigenic strains applied to soil occupy the same niches as the natural occurring toxigenic strains. They, therefore, are capable of competing and displacing toxigenic strains. In this paper, we review recent development in biological control of aflatoxin contamination.
Aflatoxins ; biosynthesis ; toxicity ; Animals ; Aspergillus ; growth & development ; pathogenicity ; physiology ; Aspergillus flavus ; growth & development ; pathogenicity ; physiology ; Food Contamination ; prevention & control ; Herbicides ; Humans ; Pest Control, Biological ; methods ; Soil Microbiology ; Species Specificity