[Characteristics of Cd Fluxe in Topsoil Around Typical Mining Area in Hezhou, Guangxi].

Guangxi is a typical geological high background area in southwest China, where carbonates, black rock series, basic-ultrabasic rock mass, and metal deposits (mineralized bodies) exhibit strong weathering into loam, resulting in higher cadmium (Cd) content in the soil than that in other areas of China. In order to investigate the degree of influence of mining activities on topsoil environmental quality in the area with high geological background, we chose a mining area and control area in Hezhou for this research and systematically carried out a comparative study on Cd transport routes and transport flux density in topsoil. The results showed that the average atmospheric dry and wet deposition flux densities of Cd in the soil of the mining area and control area were 1.87 g·(hm2·a)-1 and 1.52 g·(hm2·a)-1, accounting for 61.5% and 60.3% of the total input flux density, respectively. The flux density of Cd in the soil by fertilization and irrigation was lower. Surface water infiltration was the main avenue of soil Cd output in both the mining area and control area, accounting for 75.4% and 86.6% of the total output flux density, respectively. The harvest output flux density in the mining area was higher than that in the control area, and the Cd content of rice planted in the mining area was higher than the standard, whereas that of maize was safe. On the whole, the net transport flux densities of soil Cd in the mining area and control area were -3.05 g·(hm2·a)-1 and -4.05 g·(hm2·a)-1, both of which showed Cd leaching in the soil. However, the points of high atmospheric deposition flux density and exceeding Cd content in rice were mainly distributed around the mining area, which may have posed a potential threat to the health of local residents. Therefore, it is suggested to control the soil Cd pollution through monitoring and planting structure adjustment.

Multiple RNA Profiling Reveal Epigenetic Toxicity Effects of Oxidative Stress by Graphene Oxide Silver Nanoparticles in-vitro.

Introduction: The increasing industrial and biomedical utilization of graphene oxide silver nanoparticles (GO-AgNPs) raises the concern of nanosafety: exposure to the AgNPs or GO-AgNPs increases the generation of reactive oxygen species (ROS), causes DNA damage and alters the expression of whole transcriptome including mRNA, miRNA, tRNA, lncRNA, circRNA and others. Although the roles of different RNAs in epigenetic toxicity are being studied during the last decade, but still we have little knowledge about the role of circle RNAs (circRNAs) in epigenetic toxicity. Methods: Rabbit fetal fibroblast cells (RFFCs) were treated with 0, 8, 16, 24, 32 and 48 µg/mL GO-AgNPs to test the cell viability and 24 µg/mL GO-AgNPs was selected as the experimental dose. After 24 h treatment with 24 µg/mL GO-AgNPs, the level of ROS, malondialdehyde (MDA), superoxide dismutase (SOD), intracellular ATP, glutathione peroxidase (GPx), and glutathione reductase (Gr) were measured in the RFFCs. High-throughput whole transcriptome sequencing was performed to compare the expression of circRNAs, long non-coding RNAs (lncRNA) and mRNA between 24 µg/mL GO-AgNPs-treated RFFCs and control cells. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was performed to validate the accuracy of circRNA sequencing data. Bioinformatics analyses were performed to reveal the potential functional roles and related pathways of differentially expressed circRNAs, lncRNA and mRNA and to construct a circRNA-miRNA-mRNA interaction network. Results: We found that 57 circRNAs, 75 lncRNAs, and 444 mRNAs were upregulated while 35 circRNAs, 21 lncRNAs, and 186 mRNAs were downregulated. These differentially expressed genes are mainly involved in the transcriptional mis-regulation of cancer through several pathways: MAPK signaling pathway (circRNAs), non-homologous end-joining (lncRNAs), as well as PPAR and TGF-beta signaling pathways (mRNAs). Conclusion: These data revealed the potential roles of circRNAs in the GO-AgNPs induced toxicity through oxidative damage, which would be the basis for further research to determine their roles in the regulation of different biological processes.

Identification of circular RNAs expression pattern in caprine fetal fibroblast cells exposed to a chronic non-cytotoxic dose of graphene oxide-silver nanoparticle nanocomposites.

The widespread use of graphene oxide-silver nanoparticle nanocomposites (GO-AgNPs) in biomedical sciences is increasing the chances of human and animal exposure to its chronic non-toxic doses. Exposure to AgNPs-related nanomaterials may result in the negative effect on the dam, fetus and offspring. However, there are only little available information for profound understanding of the epigenetic alteration in the cells and animals caused by low-dose chronic exposure of GO-AgNPs. The present study investigated the effect of 0.5 µg/mL GO-AgNPs for 10 weeks on the differential expression of circular RNAs (circRNAs) in caprine fetal fibroblast cells (CFFCs), and this dose of GO-AgNPs did not affect cell viability and ROS level. We predicted the functions of those differentially expressed (DE) circRNAs in CFFCs by bioinformatics analysis. Furthermore, we validated the expression of ten DE circRNAs using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) to ensure the reliability of the sequencing data. Our results showed that the DE circRNAs may potentially regulate the GO-AgNPs-inducing epigenetic toxicity through a regulatory network consisted of circRNAs, miRNAs and messenger RNAs (mRNAs). Therefore, the epigenetics toxicity is essential to assess the biosafety level of GO-AgNPs.

Graphene Oxide-Silver Nanoparticle Nanocomposites Induce Oxidative Stress and Aberrant Methylation in Caprine Fetal Fibroblast Cells.

Graphene oxide-silver nanoparticle (GO-AgNPs) nanocomposites have drawn much attention for their potential in biomedical uses. However, the potential toxicity of GO-AgNPs in animals and humans remains unknown, particularly in the developing fetus. Here, we reported the GO-AgNP-mediated cytotoxicity and epigenetic alteration status in caprine fetal fibroblast cells (CFFCs). In brief, the proliferation and apoptosis rate of GO-AgNP-treated CFFCs (4 and 8 µg/mL of GO-AgNPs) were measured using the cell-counting kit (CCK-8) assay and the annexin V/propidium iodide (PI) assay, respectively. In addition, the oxidative stress induced by GO-AgNPs and detailed mechanisms were studied by evaluating the generation of reactive oxygen species (ROS), superoxide dismutase (SOD), lactate dehydrogenase (LDH), malondialdehyde (MDA), and caspase-3 and abnormal methylation. The expression of pro- and anti-apoptotic genes and DNA methyltransferases was measured using reverse transcription followed by RT-qPCR. Our data indicated that GO-AgNPs cause cytotoxicity in a dose-dependent manner. GO-AgNPs induced significant cytotoxicity by the loss of cell viability, production of ROS, increasing leakage of LDH and level of MDA, increasing expression of pro-apoptotic genes, and decreasing expression of anti-apoptotic genes. GO-AgNPs incited DNA hypomethylation and the decreased expression of DNMT3A. Taken together, this study showed that GO-AgNPs increase the generation of ROS and cause apoptosis and DNA hypomethylation in CFFCs. Therefore, the potential applications of GO-AgNPs in biomedicine should be re-evaluated.