Arsenic intake-induced gastric toxicity is blocked by grape skin extract by modulating inflammation and oxidative stress in a mouse model.

Arsenic (As) is known to induce toxic responses in many organs of human beings and animals. However, research concerning toxicity in the stomach is limited. In this study, arsenic-induced gastric toxicity was investigated in a mouse model, and grape skin extract (GSE) was confirmed to have protective effects against arsenic toxicity. Our experimental results showed that exposure to 10 mg/l arsenic via drinking water for 56 days caused oxidative damage and inflammatory responses. The H2O2 and malondialdehyde (MDA) contents were significantly increased, accompanied by significant decreases in total superoxide dismutase (T-SOD) activity and glutathione (GSH) content in the gastric tissue of arsenic-treated mice. Two inflammatory signalling pathways, i.e., TLR2/MyD88/NF-κB and IL-6/STAT-3, were activated, along with inflammatory cell infiltration and the elevated mRNA expression of pro-inflammatory cytokines (TNF-α, IL-1ß and IFN-γ) and myeloperoxidase (MPO) in the gastric tissue of mice exposed to arsenic. Meanwhile, the mRNA levels of the ZO-1, ZO-2 and occludin genes, which encode the key components of tight junction (TJ) complexes, were downregulated. However, the application of GSE (300 mg/kg bw) significantly inhibited the arsenic-induced increases in H2O2 and MDA contents and the decreases in T-SOD activity and GSH content. The arsenic-mediated gene expression of pro-inflammatory cytokines (TNF-α, IL-1ß and IFN-γ), MPO and IL-6/STAT3 and TLR2/MyD88/NF-κB pathways was found down-regulated. Moreover, the arsenic-induced inflammatory cell infiltration and inhibition of TJ genes transcription were markedly attenuated in the As+GSE (300 mg/kg bw) group. Based on the present findings, arsenic intake appears to cause gastric toxicity via oxidative stress and inflammation, and the application of GSE offers significant protection against arsenic toxicity in a mouse model by attenuating the oxidative stress and inflammatory response. Our results suggest that GSE by oral administration might function as a candidate therapeutic supplement to antagonize arsenic toxicity.

Exposure to PFDoA causes disruption of the hypothalamus-pituitary-thyroid axis in zebrafish larvae.

Perfluorododecanoic acid (PFDoA), a kind of perfluorinated carboxylic acid (PFCA) with 12 carbon atoms, has an extensive industrial utilization and is widespread in both wildlife and the water environment, and was reported to have the potential to cause a disruption in the thyroid hormone system homeostasis. In this study, zebrafish embryos/larvae were exposed to different concentrations of PFDoA (0, 0.24, 1.2, 6 mg/L) for 96 h post-fertilization (hpf). PFDoA exposure caused obvious growth restriction connected with the reduced thyroid hormones (THs) contents in zebrafish larvae, strengthening the interference effect on the growth of fish larvae. The transcriptional level of genes within the hypothalamic-pituitary-thyroid (HPT) axis was analyzed. The gene expression levels of thyrotropin-releasing hormone (trh) and corticotrophin-releasing hormone (crh) were upregulated upon exposure to 6 mg/L of PFDoA, and iodothyronine deiodinases (dio2) was upregulated in the 1.2 mg/L PFDoA group. The transcription of thyroglobulin (tg) and thyroid receptor (trß) were significantly downregulated upon exposure to 1.2 mg/L and 6 mg/L of PFDoA. PFDoA could also decrease the levels of sodium/iodide symporter (nis) and transthyretin (ttr) gene expression in a concentration-dependent manner after exposure. A significant decrease in thyroid-stimulating hormoneß (tshß), uridinediphosphate-glucuronosyltransferase (ugt1ab) and thyroid receptor (trα) gene expression were observed at 6 mg/L PFDoA exposure. Upregulation and downregulation of iodothyronine deiodinases (dio1) gene expression were observed upon the treatment of 1.2 mg/L and 6 mg/L PFDoA, respectively. All the data demonstrated that gene expression in the HPT axis altered after different PFDoA treatment and the potential mechanisms of the disruption of thyroid status could occur at several steps in the process of synthesis, regulation, and action of thyroid hormones.

Analyzing nutrient distribution in different particle-size municipal aged refuse.

To investigate the feasibility of using aged municipal solid waste as farmland soil, it is essential to study its nutritive compositions for plant growth. Previous studies have demonstrated that the properties of different particle-size aged refuse are very different, therefore, the present study was conducted to evaluate the adequacy of three elements (N, P, K) and the fractionation of inorganic P in the aged refuse with a particle-size distribution of 900 to 300, 300 to 150, 150 to 105, 105 to 90 and 90 to 0 µm. The results indicate that (1) total quantities of N, P, K were much larger than that in the general soil and the quantities of available N, P and K were also adequate; (2) total content of P was sufficient, but the ratio of available-P to total P was not high enough; (3) with the decrease of particle size, the contents of these elements presented different trends. The results implicate that total contents of N, P and K were enough for the aged refuse being exploited as cultivated soil, and different gradation of aged refuse could be added to improve poor soils. It provides scientific evidence for utilizing different particle-size aged refuse comprehensively.