The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Stefania Marzocco - One of the best experts on this subject based on the ideXlab platform.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells: A concentration related study. PLoS One 2012
2016Co-Authors: Bianca Fontanella, Lorella Severino, Andrea Quaroni, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5–80 mM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G0/G1 interphase and in the S phase, with a concomitant reduction in the fraction of cells in G2. Interestingly, when administered at lower concentrations (0.1–2.5 mM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results furthe
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Nivalenol induces oxidative stress and increases deoxyNivalenol pro oxidant effect in intestinal epithelial cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Marisanta Del Regno, Lorella Severino, Andrea Quaroni, Simona Adesso, Ada Popolo, Giuseppina Autore, Stefania MarzoccoAbstract:Mycotoxins are secondary fungal metabolites often found as contaminants in almost all agricultural commodities worldwide, and the consumption of food or feed contaminated by mycotoxins represents a major risk for human and animal health. Reactive oxygen species are normal products of cellular metabolism. However, disproportionate generation of reactive oxygen species poses a serious problem to bodily homeostasis and causes oxidative tissue damage. In this study we analyzed the effect of two trichothecenes mycotoxins: Nivalenol and deoxyNivalenol, alone and in combination, on oxidative stress in the non-tumorigenic intestinal epithelial cell line IEC-6. Our results indicate the pro-oxidant Nivalenol effect in IEC-6, the stronger pro-oxidant effect of Nivalenol when compared to deoxyNivalenol and, interestingly, that Nivalenol increases deoxyNivalenol pro-oxidative effects. Mechanistic studies indicate that the observed effects were mediated by NADPH oxidase, calcium homeostasis alteration, NF-kB and Nrf2 pathways activation and by iNOS and nitrotyrosine formation. The toxicological interaction by Nivalenol and deoxyNivalenol reported in this study in IEC-6, points out the importance of the toxic effect of these mycotoxins, mostly in combination, further highlighting the risk assessment process of these toxins that are of growing concern.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells a concentration related study
PLOS ONE, 2012Co-Authors: Giuseppe Bianco, Bianca Fontanella, Lorella Severino, Andrea Quaroni, Giuseppina Autore, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5-80 µM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G(0)/G(1) interphase and in the S phase, with a concomitant reduction in the fraction of cells in G(2). Interestingly, when administered at lower concentrations (0.1-2.5 µM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results further highlight the risks associated with intake of even low levels of these toxins.
Ronald D Plattner - One of the best experts on this subject based on the ideXlab platform.
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determination of deoxyNivalenol and Nivalenol in corn and wheat by liquid chromatography with electrospray mass spectrometry
Journal of AOAC International, 2003Co-Authors: Ronald D Plattner, Chris M MaragosAbstract:The fungus Fusarium graminearum is a pathogen of both wheat and corn. Strains of the fungus from the United States produce a toxin, deoxyNivalenol (DON); strains of the fungus from Asia and Europe produce DON or a related toxin, Nivalenol. These toxins can cause disease in livestock, and their po tential presence in feed and foods is a concern for animal and human health. A method was devel oped to detect both toxins in corn and wheat by liquid chromatography/mass spectrometry of an extract of ground grain. The method requires no sample cleanup and can detect the toxins at
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a genetic map of gibberella zeae fusarium graminearum
Genetics, 2002Co-Authors: James E Jurgenson, Kurt A Zeller, John F Leslie, Robert L. Bowden, Nancy J Alexander, Ronald D PlattnerAbstract:We constructed a genetic linkage map of Gibberella zeae ( Fusarium graminearum ) by crossing complementary nitrate-nonutilizing ( nit ) mutants of G. zeae strains R-5470 (from Japan) and Z-3639 (from Kansas). We selected 99 nitrate-utilizing (recombinant) progeny and analyzed them for amplified fragment length polymorphisms (AFLPs). We used 34 pairs of two-base selective AFLP primers and identified 1048 polymorphic markers that mapped to 468 unique loci on nine linkage groups. The total map length is ~1300 cM with an average interval of 2.8 map units between loci. Three of the nine linkage groups contain regions in which there are high levels of segregation distortion. Selection for the nitrate-utilizing recombinant progeny can explain two of the three skewed regions. Two linkage groups have recombination patterns that are consistent with the presence of intercalary inversions. Loci governing trichothecene toxin amount and type (deoxyNivalenol or Nivalenol) map on linkage groups IV and I, respectively. The locus governing the type of trichothecene produced (Nivalenol or deoxyNivalenol) cosegregated with the TRI5 gene (which encodes trichodiene synthase) and probably maps in the trichothecene gene cluster. This linkage map will be useful in population genetic studies, in map-based cloning, for QTL (quantitative trait loci) analysis, for ordering genomic libraries, and for genomic comparisons of related species.
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A Genetic Map of Gibberella zeae (Fusarium graminearum)
Genetics, 2002Co-Authors: James E Jurgenson, Kurt A Zeller, John F Leslie, Robert L. Bowden, Nancy J Alexander, Ronald D PlattnerAbstract:We constructed a genetic linkage map of Gibberella zeae (Fusarium graminearum) by crossing complementary nitrate-nonutilizing (nit) mutants of G. zeae strains R-5470 (from Japan) and Z-3639 (from Kansas). We selected 99 nitrate-utilizing (recombinant) progeny and analyzed them for amplified fragment length polymorphisms (AFLPs). We used 34 pairs of two-base selective AFLP primers and identified 1048 polymorphic markers that mapped to 468 unique loci on nine linkage groups. The total map length is approximately 1300 cM with an average interval of 2.8 map units between loci. Three of the nine linkage groups contain regions in which there are high levels of segregation distortion. Selection for the nitrate-utilizing recombinant progeny can explain two of the three skewed regions. Two linkage groups have recombination patterns that are consistent with the presence of intercalary inversions. Loci governing trichothecene toxin amount and type (deoxyNivalenol or Nivalenol) map on linkage groups IV and I, respectively. The locus governing the type of trichothecene produced (Nivalenol or deoxyNivalenol) cosegregated with the TRI5 gene (which encodes trichodiene synthase) and probably maps in the trichothecene gene cluster. This linkage map will be useful in population genetic studies, in map-based cloning, for QTL (quantitative trait loci) analysis, for ordering genomic libraries, and for genomic comparisons of related species.
Andrea Quaroni - One of the best experts on this subject based on the ideXlab platform.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells: A concentration related study. PLoS One 2012
2016Co-Authors: Bianca Fontanella, Lorella Severino, Andrea Quaroni, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5–80 mM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G0/G1 interphase and in the S phase, with a concomitant reduction in the fraction of cells in G2. Interestingly, when administered at lower concentrations (0.1–2.5 mM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results furthe
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Nivalenol induces oxidative stress and increases deoxyNivalenol pro oxidant effect in intestinal epithelial cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Marisanta Del Regno, Lorella Severino, Andrea Quaroni, Simona Adesso, Ada Popolo, Giuseppina Autore, Stefania MarzoccoAbstract:Mycotoxins are secondary fungal metabolites often found as contaminants in almost all agricultural commodities worldwide, and the consumption of food or feed contaminated by mycotoxins represents a major risk for human and animal health. Reactive oxygen species are normal products of cellular metabolism. However, disproportionate generation of reactive oxygen species poses a serious problem to bodily homeostasis and causes oxidative tissue damage. In this study we analyzed the effect of two trichothecenes mycotoxins: Nivalenol and deoxyNivalenol, alone and in combination, on oxidative stress in the non-tumorigenic intestinal epithelial cell line IEC-6. Our results indicate the pro-oxidant Nivalenol effect in IEC-6, the stronger pro-oxidant effect of Nivalenol when compared to deoxyNivalenol and, interestingly, that Nivalenol increases deoxyNivalenol pro-oxidative effects. Mechanistic studies indicate that the observed effects were mediated by NADPH oxidase, calcium homeostasis alteration, NF-kB and Nrf2 pathways activation and by iNOS and nitrotyrosine formation. The toxicological interaction by Nivalenol and deoxyNivalenol reported in this study in IEC-6, points out the importance of the toxic effect of these mycotoxins, mostly in combination, further highlighting the risk assessment process of these toxins that are of growing concern.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells a concentration related study
PLOS ONE, 2012Co-Authors: Giuseppe Bianco, Bianca Fontanella, Lorella Severino, Andrea Quaroni, Giuseppina Autore, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5-80 µM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G(0)/G(1) interphase and in the S phase, with a concomitant reduction in the fraction of cells in G(2). Interestingly, when administered at lower concentrations (0.1-2.5 µM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results further highlight the risks associated with intake of even low levels of these toxins.
Lorella Severino - One of the best experts on this subject based on the ideXlab platform.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells: A concentration related study. PLoS One 2012
2016Co-Authors: Bianca Fontanella, Lorella Severino, Andrea Quaroni, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5–80 mM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G0/G1 interphase and in the S phase, with a concomitant reduction in the fraction of cells in G2. Interestingly, when administered at lower concentrations (0.1–2.5 mM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results furthe
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Nivalenol induces oxidative stress and increases deoxyNivalenol pro oxidant effect in intestinal epithelial cells
Toxicology and Applied Pharmacology, 2015Co-Authors: Marisanta Del Regno, Lorella Severino, Andrea Quaroni, Simona Adesso, Ada Popolo, Giuseppina Autore, Stefania MarzoccoAbstract:Mycotoxins are secondary fungal metabolites often found as contaminants in almost all agricultural commodities worldwide, and the consumption of food or feed contaminated by mycotoxins represents a major risk for human and animal health. Reactive oxygen species are normal products of cellular metabolism. However, disproportionate generation of reactive oxygen species poses a serious problem to bodily homeostasis and causes oxidative tissue damage. In this study we analyzed the effect of two trichothecenes mycotoxins: Nivalenol and deoxyNivalenol, alone and in combination, on oxidative stress in the non-tumorigenic intestinal epithelial cell line IEC-6. Our results indicate the pro-oxidant Nivalenol effect in IEC-6, the stronger pro-oxidant effect of Nivalenol when compared to deoxyNivalenol and, interestingly, that Nivalenol increases deoxyNivalenol pro-oxidative effects. Mechanistic studies indicate that the observed effects were mediated by NADPH oxidase, calcium homeostasis alteration, NF-kB and Nrf2 pathways activation and by iNOS and nitrotyrosine formation. The toxicological interaction by Nivalenol and deoxyNivalenol reported in this study in IEC-6, points out the importance of the toxic effect of these mycotoxins, mostly in combination, further highlighting the risk assessment process of these toxins that are of growing concern.
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Nivalenol and deoxyNivalenol affect rat intestinal epithelial cells a concentration related study
PLOS ONE, 2012Co-Authors: Giuseppe Bianco, Bianca Fontanella, Lorella Severino, Andrea Quaroni, Giuseppina Autore, Stefania MarzoccoAbstract:The integrity of the gastrointestinal tract represents a crucial first level defence against ingested toxins. Among them, Nivalenol is a trichotecenes mycotoxin frequently found on cereals and processed grains; when it contaminates human food and animal feed it is often associated with another widespread contaminant, DeoxyNivalenol. Following their ingestion, intestinal epithelial cells are exposed to concentrations of these trichothecenes high enough to cause mycotoxicosis. In this study we have investigated the effects of Nivalenol and DeoxyNivalenol on intestinal cells in an in vitro model system utilizing the non-tumorigenic rat intestinal epithelial cell line IEC-6. Both Nivalenol and DeoxyNivalenol (5-80 µM) significantly affected IEC-6 viability through a pro-apoptotic process which mainly involved the following steps: (i) Bax induction; (ii) Bcl-2 inhibition, and (iii) caspase-3 activation. Moreover, treatment with Nivalenol produced a significant cell cycle arrest of IEC-6 cells, primarily at the G(0)/G(1) interphase and in the S phase, with a concomitant reduction in the fraction of cells in G(2). Interestingly, when administered at lower concentrations (0.1-2.5 µM), both Nivalenol and DeoxyNivalenol affected epithelial cell migration (restitution), representing the initial step in gastrointestinal wound healing in the gut. This reduced motility was associated with significant remodelling of the actin cytoskeleton, and changes in expression of connexin-43 and focal adhesion kinase. The concentration range of Nivalenol or DeoxyNivalenol we have tested is comparable with the mean estimated daily intake of consumers eating contaminated food. Thus, our results further highlight the risks associated with intake of even low levels of these toxins.
Masayo Kushiro - One of the best experts on this subject based on the ideXlab platform.
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effect of milling on the content of deoxyNivalenol Nivalenol and zearalenone in japanese wheat
Food Control, 2014Co-Authors: Yazhi Zheng, Hiroshi Okadome, Hiroyuki Nakagawa, Hitoshi Nagashima, Takashi Nakajima, Sharif Md Hossen, Megumi Yoshida, Yuki Sago, Masayo KushiroAbstract:Abstract The effect of milling on the content of zearalenone (ZEA), a Fusarium mycotoxin, in a semi-processed wheat product was investigated and compared with that of deoxyNivalenol (DON) or Nivalenol (NIV). Two grain samples of Japanese soft wheat varieties, norin 61 and chikugoizumi , were milled to obtain three breaking flours (1B, 2B, 3B), three middling flours (1M, 2M, 3M) and two outer-layer fractions (bran and shorts). Patent flour for human consumption was made from 1B, 1M, 2B and 2M flours, while low-grade flour for animal feed was made from 3B to 3M flours. The contents of ZEA in patent flour, low-grade flour, bran and shorts were analyzed by an in-house validated analytical method using solvent extraction, multifunctional cartridge cleanup, and HPLC-fluorescence detection. A greater than 50% reduction in ZEA was observed in the patent flour of both samples, while 4–74% reduction in DON and NIV in the patent flour of the same two samples was observed. The results of this study revealed that the transfer ratios of ZEA had different features from those of deoxyNivalenol and Nivalenol.
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distribution of Nivalenol in milling fractions of severely fusarium infected japanese soft winter wheat grains
Mycotoxins, 2012Co-Authors: Sharif Md Hossen, Hiroshi Okadome, Hiroyuki Nakagawa, Hitoshi Nagashima, Takashi Nakajima, Megumi Yoshida, Masayo KushiroAbstract:The fate of Fusarium mycotoxin Nivalenol during milling of a Japanese wheat cultivar was investigated. Grain samples with two distinct Nivalenol levels were test-milled to produce six fl our fractions (Breaking flours: 1B, 2B, and 3B, Middling flours: 1M, 2M, and 3M) and two outer layer fractions (bran and shorts). Patent flour for human consumption was made from 1B, 1M, 2B, and 2M, while low-grade flour was made from 3B and 3M. These four samples; Patent flour, low-grade flour, bran and shorts were analyzed for the content of Nivalenol by HPLC-UV. Two samples showed similar patterns of Nivalenol distribution in milling fractions.
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Distinct Distribution of DeoxyNivalenol, Nivalenol, and Ergosterol in Fusarium-infected Japanese Soft Red Winter Wheat Milling Fractions
Mycopathologia, 2011Co-Authors: Manasikan Thammawong, Hiroshi Okadome, Takeo Shiina, Hiroyuki Nakagawa, Hitoshi Nagashima, Takashi Nakajima, Masayo KushiroAbstract:The occurrence of mycotoxins in small grain cereals and their retention in final products are serious concerns for food safety. Previously, we investigated the fate of deoxyNivalenol and Nivalenol in a Japanese soft red winter wheat cultivar during milling and we found that deoxyNivalenol and/or Nivalenol was readily distributed among flours for human consumption. In the present study, we analyzed the ergosterol concentrations in the milling fractions as an index of fungal biomass to elucidate the relationship between deoxyNivalenol/Nivalenol accumulation and fungal invasion into the grain, after the in-house validation of an analytical method for quantifying ergosterol in the resulting milling fractions (patent flour, low-grade flour, bran, and shorts). Using three samples with different levels of deoxyNivalenol and/or Nivalenol contamination, the contents of deoxyNivalenol/Nivalenol and ergosterol in the resulting milling fractions were evaluated. The concentration of ergosterol was always lowest in patent flour and highest in bran or shorts, indicating that most of the fungi is retained in the outer layers of grain (bran and shorts) even in highly contaminated grain. On the other hand, the concentrations of deoxyNivalenol and Nivalenol were similar in the low-grade and patent flours and only slightly lower than in the medium-level and high-level contaminated grains. Moreover, the percentage distribution of ergosterol was higher in bran than in other fractions in all cases, which differed from that of deoxyNivalenol/Nivalenol. This result indicates the diffusion of deoxyNivalenol/Nivalenol inside the grain that is independent of fungal invasion.
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nuclear factor κb inhibitors alleviate Nivalenol induced cytotoxicity in hl60 cells
Environmental Toxicology and Pharmacology, 2011Co-Authors: Hitoshi Nagashima, Masayo Kushiro, Hiroyuki NakagawaAbstract:Abstract Tricothecene mycotoxins, such as Nivalenol, are toxic to leukocytes. To elucidate the molecular mechanism of Nivalenol toxicity, we investigated the involvement of nuclear factor-κB (NF-κB) in Nivalenol-induced cytotoxicity in HL60 cells using the NF-κB inhibitors pyrrolidinedithiocarbamate (PDTC) and dexamethasone. Cells were treated with the chemicals for 24 h before assays were performed. Nivalenol elicited interleukin (IL)-8 secretion. IL-8 secretion was lower in cells concomitantly treated with Nivalenol and NF-κB inhibitors than with Nivalenol alone. Nivalenol reduced monocyte chemotactic protein (MCP)-1 secretion. MCP-1 secretion was higher in cells concomitantly treated with Nivalenol and NF-κB inhibitors than with Nivalenol alone. NF-κB inhibitors thus alleviated the effects of Nivalenol, indicating that NF-κB is important for Nivalenol-caused changes in cytokine secretion. Nivalenol hindered cell proliferation, and dexamethasone reduced this effect, suggesting that NF-κB contributes to cell proliferation. Thus, it appears that NF-κB is involved in Nivalenol-induced toxicity in HL60 cells.
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distribution of deoxyNivalenol and Nivalenol in milling fractions from fusarium infected japanese wheat cultivars
Journal of Food Protection, 2010Co-Authors: Manasikan Thammawong, Hiroshi Okadome, Hiroyuki Nakagawa, Hitoshi Nagashima, Takashi Nakajima, Mayuko Okabe, Tomomi Kawasaki, Masayo KushiroAbstract:The fate of the Fusarium mycotoxins deoxyNivalenol and Nivalenol during the milling of Japanese wheat cultivars artificially infected with Fusarium was investigated. Grain samples with different mycotoxin concentrations were milled using a laboratory-scale test mill to produce eight fractions: three breaking flours (1B, 2B, and 3B), three reduction flours (1M, 2M, and 3M), wheat bran, and wheat shorts. Patent flour for human consumption was made from the 1B, 2B, 1M, and 2M flours, and low-grade flour was made from 3B and 3M flours. The four resulting samples (patent flour, low-grade flour, bran, and shorts) were analyzed for deoxyNivalenol and/or Nivalenol with an in-house validated analytical method using high-performance liquid chromatography with UV absorbance detection. In samples with different mycotoxin concentrations, the distribution of those toxins differed among the milling fractions. Grains with a lower level of contamination produced bran and shorts samples with a high relative concentration of Nivalenol. A high percentage of Nivalenol was found in patent flour, followed by bran. Contrary to the less-contaminated sample, the concentration of Nivalenol in moderately contaminated grain was high only in the shorts sample. The highest percentage of deoxyNivalenol and Nivalenol was observed in the patent flour. The results of this study indicate that the distribution of deoxyNivalenol and Nivalenol in milled Japanese wheat could be influenced by the contamination level of the original grain, and the milling process is not always effective for removal of toxins from wheat grains.