Mycotoxin problems are one of great concern to health scientists. Toxic fungal metabolites such as aflatoxins, trichothecenes, zearalenone and others are contaminated in our environments and induce various diseases. In this manuscript, the author will summarize the recent advances on toxicology of mycotoxins in special references to toxicological characters, cytotoxicity, genotoxicity (mutagenicity and carcinogenicity), metabolism, and biochemical mode of action. Interaction of mycotoxins with cellular components will be reviewed in order to clarify the toxicological characteristics of mycotoxins such as aflatoxins, trichothecenes, zearalenone, toxic peptides, and anthraquinoid mycotoxins.

The Pearl River in the south of China is the second largest river in China in terms of discharge volume. Two cruises were made to investigate the dynamics of nutrients and phytoplankton biomass in June and July 1998, across the Pearl River estuary to the adjacent territorial waters of Hong Kong. On-deck incubation experiments of 5 mixtures of freshwater from the surface with seawater from below the halocline were conducted to simulate time scales of phytoplankton blooms for each freshwaterheawater mixture and to examine uptake of nutrients. In July, phytoplankton growth rates increased with salinity of the mixtures, with the lowest growth rate (0.81 d-') in freshwater and the highest (2.41 d-l) in 100% seawater ( s a h i t y = 29). PO4 was lower in freshwater (0.3 PM) than in seawater (1.2 pM), whereas concentrations of NO3+ NH4 + urea (-80 FM) and SiO, (150 FM) were higher in freshwater than those in seawater (25 pM for nitrogen and 26 pM for SO,). During the incubation PO, disappeared first, indicating that P was limiting the phytoplankton biomass. All mixtures reached the maximum in phytoplankton biomass in 3 to 4 d. There was a regional maximum of phytoplankton biomass that occurred at the seaward edge of the estuarine plume during June The region moved eastwards (away from the estuary) to the southern waters between Lantau Island and Hong Kong Island during July. Mixing dagrams of NO3 and Si04 showed conservative behaviour with sabnity in the estuary. These observations suggest that dilution by freshwater outflow was a controlling factor in determining the distribution of nutrients and phytoplankton biomass in the estuary due to high flow during June and July. The regional maximum of phytoplankton biomass was comparable to that resulting from the incubation and coincided with the exhaustion of PO, during July. On the estuanne (west) side of the regonal maximum, chl a fluorescence increased during 24 h incubations, but decreased at the station with the maximum and on the east side, suggesting the possible hutation of nutrients to the phytoplankton community. In the same eastern waters, both PO, and SiO, were very low. However, NO, and NH, remained abundant, suggesting possible CO-limitation by phosphorus and silicon. We hypothesize that considerable seasonal rainfall in June and early July might have contributed an additional source of nitrogen to the water column, which resulted in the exhaustion of PO, and SiO, before nitrogen.

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Aflatoxins and their animal biotransformation products were screened for carcinogenic potential using the Ames' in vitro microbial detection system for carcinogens as bacterial mutagens [B. N. Ames et aL (1973) Proc (1). The four naturally occurring AFs, aflatoxins B1 (AFB1), B2 (AFB2), G1 (AFG1), and G2 (AFG2), when administered as mixtures, were a potent class of animal hepatocarcinogens (2-6). They have been also associated with neoplastic formations in tissues and organs other than the liver (3,(6)(7)(8)(9).Tests with rats (10) and rainbow trout (11) have revealed that AFB1 is a potent hepatocarcinogen; AFG1 is also considerably carcinogenic, but AFB2 and AFG2 possess much lower activity. Recent studies on the metabolism of AFB1 have resulted in the isolation and identification of numerous metabolites, all of minor structural variations but significantly different biological activity relative to the parent compound (12).Among these metabolites, aflatoxins Q, (AFQ1), M1 (AFM1), Bk (AFBa), and P1 (AFP1), aflatoxicol (AFL), and aflatoxicol H1 (AFLH1) (Table 1) are the biotransformation products of AFB1 when the latter is incubated with liver preparations and a NADPH-generating system (13-17). Since evidence has indicated that AFB1 requires metabolic activation for its toxic, mutagenic, and/or carcinogenic activity (18)(19)(20)(21)(22), the toxicity of each metabolite has been of great interest in the search for the active molecular species. Attempts have been made to correlate the relative activity of the different metabolic pathways and the variations in the species susceptibility to aflatoxicosis (16,23 (24,25). The analysis of the known major AF metabolites in our study permits an observation of the structureactivity relationships as related to the carcinogenic potential of the AFs. MATERIALS AND METHODSChemicals are obtained as follows: AFBI, AFG1, AFB2, and AFG2 were purchased from Makor Chemicals, Ltd., Jerusalem, Israel. AFM1, AFQ1, and AFH1 were prepared by biotransformation of AFB1 using monkey liver homogenates (14, 17). AFL was prepared by a similar biotransformation method to be published elsewhere. AFB2k and AFGk were chemically synthesized from AFB1 with dilute acid (27). AFP1 was a chemically synthesized product kindly provided by G. N. Wogan, Massachusetts Institute of Technology, Cambridge, Mass. The purity and identity of all AFs was checked by fluorodensitometric analysis of thin-layer chromatography plates and mass spectrometry. In addition, AFQ1, AFM1, AFH1, and AFB2k were checked by high-pressure liquid chromatography (28). All biochemicals, NADP+, glucose 6-phosphate, histidine, and biotin, were purchased from Sigma Chemicals, St. Louis, Mo.The bacterial tester strain, Salmonella typhimurium strain TA 98 (21), was the generous gift of B. N. Ames, University of California, Berkeley. The bacteria were stored and grown as outlined by McCann et al. (21). The hepatic S-9 enzyme preparation was prepared from Charles River male white rats (200-250 g) and utilized according to procedur...

Epidemiologic studies linking high serum iron with cancer risks are limited and inconclusive, despite evidence implicating body iron in human carcinogenesis. A cohort of 309,443 adults in Taiwan who had no history of cancer had serum iron levels tested at the time of recruitment (1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008). Initially measured iron levels were associated with subsequent cancer risk by linking individuals with the National Cancer Registry and National Death File. HRs were calculated by the Cox model. One third of males (35%) and one fifth of females (18%) had high serum iron (!120 mg/dL), which was associated with a 25% increase in risk for incidence of all cancers [HR, 1.25; 95% confidence interval (CI), 1.16-1.35] and with a 39% increase in risk for mortality from all cancers (HR, 1.39; 95% CI, 1.23-1.57). The relationship between serum iron and cancer risk was a J-shaped one, with higher cancer risk at both ends, either at lower than 60 mg/dL or higher than 120 mg/dL. At the higher end, cancer risk increased by 4% for every 10 mg/dL increment above 80 mg/dL, showing a dose-response relationship, with 60 to 79 mg/dL as a reference level. In a sensitivity analysis, the increases in risk were still observed after the first 5 years of cancer cases were excluded. Liver cancer risk was increased in HBV (À) non-hepatitis B carrier (3-fold) and HBV (þ) hepatitis B carrier (24-fold). Lifestyle risks such as smoking, drinking, or inactivity interacted synergistically with high serum iron and significantly increased the cancer risks. The liver (HR, 2.49; 95% CI, 1.97-3.16) and the breast (HR, 1.31; 95% CI, 1.01-1.70) were the two major cancer sites where significant cancer risks were observed for serum iron either !120 mg/dL or !140 mg/dL, respectively. This study reveals that high serum iron is both a common disorder and a marker of increased risk for several cancers. Cancer Res; 74(22); 6589-97. Ó2014 AACR.