Pollution Characteristics and Risk Assessment of Heavy Metals in the Sediments of the Inflow Rivers of Dianchi Lake, China.

To explore the contamination status and identify the source of the heavy metals in the sediments in the major inflow rivers of Dianchi Lake in China, sediment samples were collected and analyzed. Specifically, the distribution, source, water quality, and health risk assessment of the heavy metals were analyzed using correlation analysis (CA), principal component analysis (PCA), the heavy metal contamination factor (Cf), the pollution load index (PLI), and the potential ecological risk index (PERI). Additionally, the chemical fractions were analyzed for mobility characteristics. The results indicate that the average concentration of the heavy metals in the sediment ranked in the descending order of Zn > Cr > Cu > Pb > As > Ni > Cd > Hg, and most of the elements existed in less-mobile forms. The Cfwas in the order of Hg > Zn > Cd > As > Pb > Cr > Ni; the accumulation of Hg, Zn, Cd, and As was obvious. Although the spatial variability of the heavy metal contents was pronounced, the synthetical evaluation index of the PLI and PERI both reached a high pollution level. The PCA and CA results indicate that industrial, transportation, and agricultural emissions were the dominant factors causing heavy metal pollution. These results provide important data for improving water resource management efficiency and heavy metal pollution prevention in Dianchi Lake.

3-Acetyldeoxynivalenol induces apoptosis, barrier dysfunction and endoplasmic reticulum stress by inhibiting mTORC1-dependent autophagy in porcine enterocytes.

3-Acetyldeoxynivalenol (3-Ac-DON), an acetylated form of deoxynivalenol, is widely present in mycotoxin-contaminated food, feed as well as in other natural sources. Ingestion of 3-Ac-DON may result in intestinal dysfunction, leading to gut diseases in humans and animals. Nevertheless, the molecular mechanism of 3-Ac-DON in intestinal epithelial cytotoxicity remains unclear. In this study, intestinal porcine epithelial cell line 1 (IPEC-1) cells were treated with different concentrations of 3-Ac-DON for 12 h or 24 h, respectively. The results showed that 3-Ac-DON caused decreased cell viability, cell cycle arrest in G1 phase and depolarization of mitochondrial membrane potential. Western blotting analysis showed that 3-Ac-DON significantly decreased the expression of tight junction proteins, inhibited autophagy and activated endoplasmic reticulum (ER) stress in IPEC-1 cells (P < 0.05). Further investigation demonstrated that 3-Ac-DON caused apoptosis, ER stress and barrier dysfunction were reversed after co-treatment with the autophagy activator rapamycin (100 nM), indicating that autophagy plays a key role in the process of 3-Ac-DON-induced cell damage. In addition, we demonstrated that 3-Ac-DON inhibits the occurrence of autophagy mediated by mTORC1 protein. In conclusion, our research indicated that the mTORC1 protein and autophagy played a key role in the 3-Ac-DON-induced cytotoxic in IPEC-1 cells, which would provide new therapeutic targets and ideas for 3-Ac-DON-mediated intestinal injury.