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The bioavailability of copper in contaminated soils has received more attention due to the safety concern of food chain. The bioavailability of metals is determined by its fractions which are affected by the soil properties and its aging time. This paper focused on the aging effect on the bioavailability of copper added to the soil. The garden soil (fluvo aquic soil) was treated with 100 mg/kg and 1000 mg/kg of copper(II) sulfate and incubated for 14, 21, 28, 42, 63, 120, 200, 300 and 400 days in the laboratory respectively. The sequential extraction procedure was used to characterize copper bioavailability in the soil. Meanwhile, the barley was cultured on the same soil incubated and its toxicity was assessed according to the guideline of International Organization for Standardization. The findings show that the exchangeable and carbonate-bound copper decreased with the aging time after addition of copper(II) sulfate to soil. Meanwhile, the percentages of Fe-Mn oxides-and organic-bound copper increased. The residual copper was changed little during the aging course. The copper fractions became stable in soils after 60 days. The kinetic equations showed that the Power function and the Elovich equation were well fitted to the experimental data, and the r 2 values ranged from 0.840 to 0.982 and 0.741 to 0.975, respectively. The barley test showed that the barley root length was more sensitive to reflect copper toxicity than the shoot biomass, and the exchangeable and carbonate-bound copper were significantly correlated with the barley root length.

As the number of reported deoxynivalenol (DON) contamination incidents increased steadily over the past decades, there has been a widespread interest in understanding the cellular mechanisms of the toxicological effects of DON using in vitro systems and omics technologies. The present investigation was conducted to understand the metabolomic changes in human hepatocellular carcinoma cells (HepG2) exposed to 10 μM DON for short term (4 h) and long term (12 h) periods, using a non-targeted metabolomics approach. Our results revealed a remarkable metabolic shift from short term to long term exposure to DON in HepG2 cells. Our metabolomics data also confirmed the role of DON induced oxidative stress in DON toxicity. Coupled with pattern recognition and pathway analysis, effects of DON on redox homeostasis, energy balance, lipid metabolism, and potential toxicological mechanisms were discussed, which would facilitate further studies on the risk assessment of the dietary mycotoxin DON.