Search

Fusarium species infect the major cereals consumed as food and feed, contaminating them with various toxic secondary metabolites known as toxins. Among these toxins, which include trichothecenes, zearalenone (ZEA), and fumonisins, the type-B trichothecene deoxynivalenol (DON) is generally considered as the most important. The present study evaluates an analytical method for the detection and quantification of multiple Fusarium toxins, namely, DON, acetyl forms of DON (3-Ac-DON and 15-Ac-DON), a glycoside form of DON (DON-3G), and other Fusarium toxins (nivalenol, an acetyl form of NIV (fusarenonX), T-2 and HT-2 toxins, diacetoxyscirpenol, and ZEA) in Job's tears and buckwheat.

We examined whether the analytical method of patulin (a mycotoxin found in fruit juice) developed in Nagano prefecture meets the criteria in the Codex Procedural Manual and Guidelines on Analytical Terminology. The trueness, repeatability, within-laboratory reproducibility and HorRat value were 98.8-103.4%, less than 6.4, 8.1 and 0.4%, respectively, for apple juice and pear juice.Thus, the trueness and precision met the required criteria.

PRC2 genes were analyzed for their number of gene duplications, dN/dS ratios and expression patterns among Brassicaceae and Gramineae species. Although both amino acid sequences and copy number of the PRC2 genes were generally well conserved in both Brassicaceae and Gramineae species, we observed that some rapidly evolving genes experienced duplications and expression pattern changes. After multiple duplication events, all but one or two of the duplicated copies tend to be silenced. Silenced copies were reactivated in the endosperm and showed ectopic expression in developing seeds. The results indicated that rapid evolution of some PRC2 genes is initially caused by a relaxation of selective constraint following the gene duplication events. Several loci could become maternally expressed imprinted genes and acquired functional roles in the endosperm.

We recently successfully discriminated mouse genotoxic hepatocarcinogens from non-genotoxic hepatocarcinogens via selected gene expression profiling in the mouse liver based on quantitative real-time PCR (qPCR) and statistical analysis using principal component analysis (PCA). In the present study, we applied these candidate marker genes to rat hepatocarcinogens in the rat liver. qPCR analysis of 33 genes was conducted on liver samples from groups of 4 male 4-week-old F344 rats at 4 and 48 h after a single oral administration of chemicals [2 genotoxic hepatocarcinogens: diethylnitrosamine and 2,6-dinitrotoluene; a non-genotoxic hepatocarcinogen: di(2-ethylhexyl)phthalate; and a non-genotoxic non-hepatocarcinogen: phenacetin]. Thirty-two genes exhibited significant changes in their gene expression ratios (experimental group/control group) according to statistical analysis using the Williams' test and the Dunnett's test. The changes appeared to be greater at 4h than at 48 h. Finally, statistical analysis via PCA successfully differentiated the genotoxic hepatocarcinogens from the non-genotoxic hepatocarcinogen and the non-genotoxic non-hepatocarcinogen at 4h based on 16 genes (Ccnf, Ccng1, Cyp4a10, Ddit4l, Egfr, Gadd45g, Gdf15, Hspb1, Igfbp1, Jun, Myc, Net1, Phlda3, Pml, Rcan1 and Tubb2c) and at 48 h based on 10 genes (Aen, Ccng1, Cdkn1a, Cyp21a1, Cyp4a10, Gdf15, Igfbp1, Mdm2, Phlda3 and Pmm1). Eight major biological processes were extracted from a gene ontology analysis: apoptosis, the cell cycle, cell proliferation, DNA damage, DNA repair, oxidative stress, oncogenes and tumor suppression. The major, biologically relevant gene pathway suggested was the DNA damage response, which signals through a Tp53-mediated pathway and leads to the induction of apoptosis. Immunohistochemical analyses for the expression of Cdkn1a and Hmox1 proteins and the level of apoptosis measured by the TUNEL assay in the liver confirmed the aforementioned results. The present results showed that mouse candidate marker genes are applicable for differentiating genotoxic hepatocarcinogens from non-genotoxic hepatocarcinogens examined in this paper in the rat liver.