Sixteen samples of Vietnamese coffee beans were examined for the presence of mycotoxigenic fungi that produce ochratoxins and fumonisins. Species of the strains isolated from the beans were tentatively identified by morphology as Aspergillus niger species complex (isolation frequencies of the beans: 56.6%), Aspergillus carbonarius (3.3%), and Aspergillus species in section Circumdati (2.9%). The strains randomly selected from the species were correctly identified by sequencing of the β-tubulin and/or mitochondrial cytochrome b gene. All of the strains of A. carbonarius and Aspergillus westerdijkiae, identified in section Circumdati, produced ochratoxin A (OTA). On the other hand, only one out of the 41 strains of A. niger produced a detectable level of OTA. Therefore, A. carbonarius and A. westerdijkiae, rather than A. niger, are likely to be the main sources of OTA contamination in the beans. With regard to A. niger, 37 out of the 41 strains produced fumonsin B2 (FB2). LC-MS/MS analysis of the 16 bean samples showed that 3 samples were contaminated with OTA and/or FB2; one Arabica sample with OTA (2.3 µg/kg), another with FB2 (55 µg/kg), and one Robusta sample with both OTA (6.3 µg/kg) and FB2 (49 µg/kg). These results demonstrate that Vietnamese coffee beans are commonly infected with OTA- and FB2-producing fungi and occasionally co-contaminated with these mycotoxins.
Fusarium graminearum causes a disease of wheat and barley known as Fusarium head blight. It contaminates the grains with trichothecene mycotoxins such as deoxynivalenol (DON). As shunt intermediates in the DON biosynthetic pathway, 7-hydroxyisotrichodermin (7-HIT) and 8-hydroxyisotrichodermin (8-HIT) are known. However, their activities have not been previously evaluated. In this study, we performed toxicity assays of these trichothecenes by using a sensitive yeast bioassay that we have recently established. The IC50 of 7-HIT and 8-HIT were in the range of 20-40 μg/ml, while the IC50 of DON was approximately 1.5 μg/ml. Although the toxicity of these shunt metabolites remains to be investigated in animal systems, our present data indicate that 7-HIT and 8-HIT may not be major issues that require regulation in agricultural products.
The toxicity of nivalenol (NIV) to the human promyelocyte-derived cell line HL60 is reviewed. NIV cytotoxicity was examined after 24 h treatment, and the inhibitor studies were performed. Cells treated with 3 μg/mL or higher NIV were damaged, and more than half of the cells appeared dead. Regarding cell proliferation, the value of 50 % inhibitory concentration of NIV was 0.16 μg/mL. Apparent DNA ladders were observed, showing that NIV induces apoptosis. Concentrations of NIV-caused morphologic damage are in accordance with DNA fragmentation, indicating that marked NIV-caused morphologic change is due to apoptosis. NIV increased interleukin-8 (IL-8/CXCL8) secretion. Conversely, NIV decreased the secretions of other cytokines monocyte chemotactic protein-1 (MCP-1/CCL2), macrophage inflammatory protein-1α (MIP-1α/CCL3), MIP-1β/CCL4, and regulated upon activation, normal T cell expressed and presumably secreted (RANTES/CCL5) concentration-dependently. That intracellular calcium ion chelator BAPTAAM mitigated the cytotoxicity of NIV indicates that this effect is dependent on intracellular calcium ion. The results of an intracellular calcium ion modulator ryanodine receptor (RyR)1-specific inhibitor dantrolene treatment indicates that RyR1 contributes to NIV-induced toxicity. Stress-activated mitogen-activated protein kinases (SAPKs), c-Jun N-terminal kinases (JNKs) and p38s, occupy the crucial positions in NIV-associated retardation of cell proliferation and IL-8 secretion. Transcription factor nuclear factor-κB (NF-κB) inhibitors reduced NIV’s effects, indicating that NF-κB is an important factor for exerting NIV toxicity. Regarding cell proliferation, no protective effect of geldanamycin, a molecular chaperone heat shock protein 90 (Hsp90)-specific inhibitor, was observed. Alternatively, Hsp90 appears to play a role in NIV-associated changes in cytokine secretions.
"Yellow rice" is the collective name of rice grains contaminated by Penicillum fungi in Japan. Three kinds of yellow rice, which are caused by different sub-species of toxigenic fungi, are known. Initially, mal-nutrition resulting from Asian poverty was regarded as the source of illness in people; however, thanks to ongoing research, the close relationship of "Shoshin-kakke (heart-attacking paralysis)", "mycotoxin", and "rice" was elucidated. Subsequently, the illness was shown to derive from "yellow rice", which was due to grains damaged by Penicillium spp. After World War II, another two kinds of yellow rice, "Islandia yellow rice" and "Citrinum yellow rice", were found, and the causative toxic compounds were determined through interdisciplinary collaborative studies. This article summarized the researches on toxigenic fungi adherent to rice and three kinds of yellow rice identified in Japan.
Food Safety Commission of Japan (FSCJ) conducted a risk assessment of aflatoxin M1 in milk and aflatoxin B1 in feeds in response to the requests of the Ministry of Health, Labour and Welfare (MHLW) and Ministry of Agriculture, Forestry, and Fisheries (MAFF), respectively. As a consequence, FSCJ concluded that the potential of AFB1 in formula feeds to exert adverse effects on human health through milk or other livestock products is extremely low. However, considering that AFM1 and some of its metabolite possibly contained in livestock products are genotoxic carcinogens, the AFB1 contamination in feeds and the AFM1 contamination in milk need to be suppressed to an ALARA (as low as reasonably achievable) level.
Hokkaido is the highest wheat production region in Japan. Fusarium head blight (FHB) has been common in the region, and occasionally damages production. In 2002, the Japanese government set a provisional regulatory limit for the mycotoxin deoxynivalenol (DON) that is produced by FHB in wheat. Since then, FHB has become the most important disease in wheat production in Hokkaido. A serious effort has been made to prevent DON contamination in wheat in order to assure food safety. This report reviews the current status of FHB in wheat, and effective methods that have been identified for reducing FHB and DON levels in Hokkaido. In addition, we present some recent findings about DON contamination in normal looking kernels, and risks for nivalenol contamination in wheat.
Rice false smut fungus (Villosiclava virens) causes smut-like disease on the panicles of rice plants. The disease development process after the booting stage has been revealed by artificial inoculation of the fungus. However, its life cycle and infection route in the field before the booting stage remain unclear. Here, these parameters are studied by referring to previous studies, morphological features of the fungus, and life cycles of phylogenetically related-fungi.
In order to clarify changes in forage rice fumonisin concentrations, we carried out field cultivation of forage rice cultivars and inoculations of forage rice with fumonisin-producing fungi. We cultivated four forage rice cultivars in Japan in 2011 and 2012. After heading, the rice was sampled every week or two weeks. The sampled biomass was separated into two parts: stems and leaves, and heads. The fumonisin concentrations in the stems and leaves were lower than those in the heads. In the heads, the fumonisin concentrations 30 days after heading were less than 10 μg/kg dry matter. However, by 40 days after heading, the fumonisin concentration began to increase, reaching its maximum around 40 to 70 days after heading. Although the maximum concentration differed among the cultivars, the trend did not differ. Fusarium fujikuroi was inoculated on rice just after heading, and we sampled heads at the yellow-ripe and full-ripe stages. Fumonisin concentrations were found to be substantially higher in the heads of inoculated plants than in the stems and leaves, especially at the full-ripe stage. On the other hand, fumonisin concentrations in control plants and in plants grown beside inoculated plants were not detectable. These results suggest that the fungus primarily infects plants shortly after the heading stage, and that fumonisin concentrations in rice heads increase after the yellow-ripe stage.
Reactive oxygen species (ROS) are high reactive compounds, which are produced on the process of oxygen consumption in aerobic organisms. ROS can be vanished by several enzymes, but excess of ROS cause damage on the organisms by the oxidation of DNA, proteins and lipids and so on. In this short review, you will see the general information about ROS (how and where ROS are produced and vanished), and then our resent reports, which show the involvement of His-Asp phosphorelay signal transductions into the control of ROS production in Aspergillus nidulans.
Mycotoxins and phytotoxins are fungal secondary metabolites that exert toxicity against complex animals (including humans) and plants, respectively. They were originally categorized as distinct toxic chemicals; however, this is now considered an inappropriate classification for toxins from plant pathogenic fungi. Fumonisins (mycotoxin) and AAL-toxins (phytotoxin) are produced by Fusarium and Alternaria pathogens, respectively, and they share a common chemical structure and biological activity. It is therefore possible that the biosynthetic pathways of the two toxins have a common evolutionary origin. Comparative studies are therefore important to determine the molecular mechanisms behind the evolution and diversification of fungal secondary metabolites. Recent development of fungal genomics and functional analysis of fungal genes could help shed light on the relationship between mycotoxins and phytotoxins. Such studies will contribute to both basic and applied research in a variety of scientific and technical fields.