Toxic effects of mycotoxins in humans. (1/28)

Mycotoxicoses are diseases caused by mycotoxins, i.e. secondary metabolites of moulds. Although they occur more frequently in areas with a hot and humid climate, favourable for the growth of moulds, they can also be found in temperate zones. Exposure to mycotoxins is mostly by ingestion, but also occurs by the dermal and inhalation routes. Mycotoxicoses often remain unrecognized by medical professionals, except when large numbers of people are involved. The present article reviews outbreaks of mycotoxicoses where the mycotoxic etiology of the disease is supported by mycotoxin analysis or identification of mycotoxin-producing fungi. Epidemiological, clinical and histological findings (when available) in outbreaks of mycotoxicoses resulting from exposure to aflatoxins, ergot, trichothecenes, ochratoxins, 3-nitropropionic acid, zearalenone and fumonisins are discussed.  (+info)

Molecular dosimetry of urinary aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China. (2/28)

Hepatocellular carcinoma is one of the five leading human cancers causing at least 250,000 deaths each year. One of the major risk factors for this disease is exposure to dietary aflatoxins, and the development of appropriate molecular dosimetry biomarkers would facilitate the identification of individuals at risk. This study was undertaken to explore the relationship between dietary intake of aflatoxins and the excretion of the major aflatoxin-DNA adduct and other metabolites into the urine of chronically exposed people. The following protocol was developed for this investigation in Guangxi Autonomous Region, People's Republic of China, where the diets of 30 males and 12 females (ages, 25-64 years) were monitored for 1 week and aflatoxin intake levels determined each day. Starting on the fourth day, total urine volumes were obtained in consecutive 12-h fractions for 3 or 4 days. High performance liquid chromatography and competitive radioimmunoassay analyses were done on each of the urine samples, and the relationships between excretion of total aflatoxin metabolites, aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, and aflatoxin B1, and aflatoxin B1 intake values were determined. The average intake of aflatoxin B1 by men was 48.4 micrograms/day, giving a total mean exposure during the study period of 276.8 micrograms. The average daily intake by women was 77.4 micrograms/day, resulting in a total average exposure during the 7-day period of 542.6 micrograms aflatoxin B1. Initial efforts to characterize aflatoxin metabolites in urine samples were with an analysis by competitive radioimmunoassay. The analysis by linear regression of the association between aflatoxin B1 intake/day and total aflatoxin metabolite excretion/day showed a correlation coefficient of only 0.26. These findings stimulated the immunoaffinity/analytical high performance liquid chromatography analysis for individual metabolites. When the data were analyzed by linear regression analysis, the aflatoxin N7-guanine excretion and aflatoxin B1 intake from the previous day showed a correlation coefficient of 0.65 and P less than 0.000001. Similar analysis for aflatoxin M1 resulted in a correlation coefficient of 0.55 and P less than 0.00001, whereas there was no positive statistical association between exposure in the diet and aflatoxin P1 excretion, despite aflatoxin P1 being quantitatively a major metabolite. Analysis of the total aflatoxin-N7-guanine excretion in the urine during the complete collection period plotted against the total aflatoxin B1 exposure in the diet for each of the individuals, smoothing the day to day variations, revealed a correlation coefficient of 0.80 and P less than 0.0000001.(ABSTRACT TRUNCATED AT 400 WORDS)  (+info)

Measurement of aflatoxin and aflatoxin metabolites in urine by liquid chromatography-tandem mass spectrometry. (3/28)

Automated immunoaffinity solid-phase extraction followed by liquid chromatography-tandem mass spectrometry and chemical analogue internal standardization is employed to detect and quantify the aflatoxins AFB(1), AFB(2), AFG(1), AFG(2), and the metabolites AFM(1) and AFP(1) in urine. The dynamic range of the method is nearly three orders of magnitude with limits of detection in the low femtogram on column range. The method was validated over a 12-day period by eight analysts. This method is suitable for agricultural, forensic, and public health laboratories during an accidental outbreak or a chemical terrorism event where a rapid and accurate diagnosis of aflatoxicosis is needed.  (+info)

Aflatoxin M1 contamination in raw bulk milk and the presence of aflatoxin B1 in corn supplied to dairy cattle in Japan. (4/28)

Aflatoxin M1 (AFM1) is a hydroxylated metabolite of aflatoxin B1 (AFB1), which has been found in the milk of dairy cattle fed AFB1-contaminated feeds. Since AFM1 has been evaluated as a possible human carcinogen, the cancer risk arising from AFM1 contamination in milk is a serious problem in food safety. To evaluate the risk of AFM1 contamination in milk, it is necessary to analyze the risk factors of AFB1 contamination in corn provided for concentrated feed in Japan. The AFM1 level in domestic raw bulk milk was measured at three sampling times, January, February and June in 2004. The AFB1 contamination in corn supplied to cows was determined at the same time as the sampling of raw milk. The AFM1 contamination levels in milk in January, February and June 2004 were 0.011, 0.007 and 0.005 ng/g, respectively. The AFB1 contamination level in the corn of the concentrated feed was higher from October of 2003 to February of 2004 than from April to June in 2004. This study provides evidence that AFM1 contamination level in milk is parallel to that of AFB1 in corn of concentrated feed, so monitoring of the AFB1 level in corn is important to prevent the risk of AFM1 contamination in milk in Japan.  (+info)

Occurrence of aflatoxin M(1) and exposure assessment in Catalonia (Spain). (5/28)

 (+info)

Effects of mycotoxins on chemiluminescent response and cytokine mRNA expression of bovine neutrophils. (6/28)

The effects of aflatoxin B(1) (AFB(1)), aflatoxin M(1) (AFM(1)), deoxynivalenol (DON) and zearalenone (ZEA) on the viability, chemiluminescent (CL) response and expression of cytokine mRNA of bovine neutrophils (PMNs) were evaluated. The opsonized zymosan (OPZ)-stimulated CL response of PMNs was significantly (P < 0.05) decreased by AFB(1) ( > 50 pg/ml), AFM(1) ( > 50 pg/ml) and ZEA (>50 pg/ml). The phorbol myristate acetate (PMA)-stimulated CL response PMNs was significantly (P < 0.05) decreased by AFB(1) (> 0.5 pg/ml), AFM(1) (> 50 pg/ml), ZEA (> 500 pg/ml) and DON ( > 5 pg/ml). Treatment with AFB(1) resulted in reduction in the mRNA expression of interleukin-1beta and tumor necrosis factor-alpha of PMNs stimulated with OPZ and PMA. These results suggest that these four mycotoxins have inhibitory effects on the function of bovine PMNs.  (+info)

Biological reactive intermediates of bisfuranoid mycotoxins. (7/28)

Based on the mode of action of AFB1 and the activities of its biologically active intermediates, one may conclude that: 1. The mode of toxic action of the bisfuranoid mycotoxin is through epoxidation of the vinyl ether double bond of their dihydrobisfuran functionality. 2. The DNA and plasma albumin adducts formed in vivo may be useful in the molecular dosimetry of these environmental carcinogens. 3. Monitoring of these adducts of AFB1 in biological samples so far indicates that aflatoxin is likely involved in the etiology of human liver cancer.  (+info)

Aflatoxin B1 and M1 contamination of animal feeds and milk from urban centers in Kenya. (8/28)

BACKGROUND: Aflatoxin M1 (AFM1) is the principal hydroxylated AFB1 metabolite present in milk of cows fed with a diet contaminated with AFB1and excreted within 12 hours of administration of contaminated feeds. OBJECTIVE: This study was initiated to assess the knowledge and practices of urban dairy farmers and feed millers about aflatoxin in feeds and milk, determine the prevalence and quantify the levels of AFB1 and AFM1 in animal feeds and milk respectively from urban environs in Kenya. METHODS: This work was carried out in the Department of Public Health Pharmacology and Toxicology, University of Nairobi, Kenya, between February 2006 and March 2007. RESULTS: A total of 830 animal feed and 613 milk samples from four urban centers were analyzed for aflatoxin B1 and M1 respectively using competitive enzyme immunoassay. Eighty six percent (353/412) of the feed samples from farmers were positive for aflatoxin B1 and 67% (235/353) of these exceeded the FAO/WHO level of 5micro gKg-1. Eighty one percent (197/243) of the feed samples from feed millers and 87% (153/175) from agrochemical shops were positive, while 58% (115/197) and 66% (92/153) of the positive samples exceeded the FAO/WHO limits respectively. Seventy two percent (315/439) of the milk from dairy farmers, 84% (71/85) from large and medium scale farmers and 99% (88/89) of the pasteurized marketed milk were positive for aflatoxin M1, and 20%, 35% an 31% of positive milk from dairy farmers, medium and large scale farmers and market outlets respectively, exceeded the WHO/FAO levels of 0.05micro g/Kg-1. Sixty seven percent of the urban smallholder dairy farmers had no knowledge that milk could be contaminated with aflatoxin M1 and neither knew how they could mitigate against this exposure. Feed millers knew about aflatoxin B1 in grains and excretion of aflatoxin M1 in milk, but were not alleviating exposure to animals. CONCLUSION: There is need to create awareness and establish routine monitoring of animal feeds and milk to reduce animal and consequently human response.  (+info)

• 1
• 2
• 3
• 4