資訊中心 > 產品文獻集 > Safety Assessment (22)

  ✔本篇論文使用華聯產品:Mouse OneArray  
 Molecular Medicine Reports. 2015, 11(2):887-95. doi: 10.3892/mmr.2014.2823.
 Biological effect of ketamine in urothelial cell lines and global gene expression analysis in the bladders of ketamine‑injected mice 
 Cheng‑huang Shen, Shou‑tsung Wang, Ying‑ray Lee, Shiau‑yuan Liu, Yi‑zhen Li, Jiann‑der Wu, Yi‑ju Chen, Yi‑wen Liu
  Abstract
Ketamine is used clinically for anesthesia but is also abused as a recreational drug. Previously, it has been established that ketamine‑induced bladder interstitial cystitis is a common syndrome in ketamine‑abusing individuals. As the mechanisms underlying ketamine‑induced cystitis have yet to be revealed, the present study investigated the effect of ketamine on human urothelial cell lines and utilized a ketamine‑injected mouse model to identify ketamine‑induced changes in gene expression in mice bladders. In the in vitro bladder cell line assay, ketamine induced cytotoxicity in a dose‑ and time‑dependent manner. Ketamine arrested the cells in G1 phase and increased the sub‑G1 population, and also increased the barrier permeability of these cell lines. In the ketamine‑injected mouse model, ketamine did not change the body weight and bladder histology of the animals at the dose of 30 mg/kg/day for 60 days. Global gene expression analysis of the animals' bladders following data screening identified ten upregulated genes and 36 downregulated genes induced by ketamine. A total of 52% of keratin family genes were downregulated, particularly keratin 6a, 13 and 14, which was confirmed by polymerase chain reaction analysis. Keratin 14 protein, one of the 36 ketamine‑induced downregulated genes, was also reduced in the ketamine‑treated mouse bladder, as determined by immunohistochemical analysis. This suggested that cytotoxicity and keratin gene downregulation may have a critical role in ketamine‑induced cystitis.
   

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  ✔本篇論文使用華聯產品:Human OneArray  
 Toxicology Research. 2015, 4, 365-375. doi: 10.1039/C4TX00181H.
 A gene signature for gold nanoparticle-exposed human cell lines
 
 
 Ruei-yue Liang, Hsin-fang Tu, Xiaotong Tan, Yu-shan Yeh, Pin Ju Chueh, Show-mei Chuang
  Abstract
There is currently a significant need for effective methods aimed at diagnosing and screening for nanoparticle exposure. We previously investigated the toxicity of three different particle sized gold nanoparticles (AuNPs) toward different types of mammalian cells and explored a related gene expression profile by cDNA microarray analysis of AuNP-exposed MRC-5 cells. In this study, we sought to further identify genes that could be used as biomarkers for AuNP exposure. We used cDNA microarray analysis to obtain comprehensive gene expression profiles from A549 cells exposed to three different-sized AuNPs. A total of 409 genes were commonly up-regulated by the tested AuNPs; of them, 71 had previously been analyzed to be up-regulated in MRC-5 cells. Among the top-ranked 30 of these 71 up-regulated genes, based on the magnitude of induction, nine genes were confirmed to be transcriptionally induced in A549 cells by all three tested AuNPs, as assessed by quantitative real-time polymerase chain reaction (qPCR). Among them, TSC22D3, TRIB3, PCK2 and DDIT4 were the most sensitive to the three AuNPs, and showed dose-dependent changes in several human cell lines. qPCR and immunoblotting analyses revealed that the same concentrations of micro-Au and nano-TiO2 failed to elicit up-regulation of these four genes at the mRNA and protein levels in any tested cell lines. Although the definition and practical implementation of specific biomarkers for nanoparticles is still in its infancy, our data suggest that it may be possible to define reliable biomarkers for the diagnosis of nanomaterial exposure.
   

  ✔本篇論文使用華聯產品:Mouse&Rat miRNA OneArray  
 Environmental Toxicology. 2015, 30(6):712-23. doi: 10.1002/tox.21949.
 Prenatal and neonatal exposure to perfluorooctane sulfonic acid results in aberrant changes in miRNA expression profile and levels in developing rat livers
 
 
 Fan Wang, Yihe Jin, Faqi Wang, Junsheng Ma, Wei Liu
  Abstract
Perfluorooctane sulfonate (PFOS) is an animal carcinogen. However, the underlying mechanism in cancer initiation is still largely unknown. Recently identified microRNAs (miRNAs) may play an important role in toxicant exposure and in the process of toxicant-induced tumorigenesis. We used PFOS to investigate PFOS-induced changes in miRNA expression in developing rat liver and the potential mechanism of PFOS-induced toxic action. Dams received 3.2 mg/kg PFOS in their feed from gestational day 1 (GD1) to postnatal day 7 (PND 7). Pups then had free access to treated feed until PND 7. We isolated RNAs from liver tissues on PND 1 and 7 and analyzed the expression profiles of 387 known rat miRNAs using microarray technology. PFOS exposure induced significant changes in miRNA expression profiles. Forty-six miRNAs had significant expression alterations on PND 1, nine miRNAs on PND 7. Specifically, expression of four miRNAs was up-regulated on PND 7 but down-regulated on PND1 (p < 0.05). Many aberrantly expressed miRNAs were related to various cancers. We found oncogenic and tumor-suppressing miRNAs, which included miR-19b, miR-21*, miR-17-3p, miR-125a-3p, miR-16, miR-26a, miR-1, miR-200c, and miR-451. In addition, four miRNAs were simultaneous significantly expressed on both PND 1 and 7. Functional Annotation analysis of the predicted transcript targets revealed that PFOS exposure potentially alters pathways associated with different cancers (cancer, melanoma, pancreatic cancer, colorectal cancer, and glioma), biological processes which include positive regulation of apoptosis and cell proliferation. Results showed PFOS exposure altered the expression of a suite of miRNAs.
   

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  ✔本篇論文使用華聯產品:Mouse OneArray  
 International Journal Of Molecular Sciences. doi:10.3390/ijms17010098.
 Optimizing a Male Reproductive Aging Mouse Model by d-Galactose Injection
 
 
 
  Abstract
The d-galactose (d-gal)-injected animal model, which is typically established by administering consecutive subcutaneous d-gal injections to animals for approximately six or eight weeks, has been frequently used for aging research. In addition, this animal model has been demonstrated to accelerate aging in the brain, kidneys, liver and blood cells. However, studies on aging in male reproductive organs that have used this animal model remain few. Therefore, the current study aimed to optimize a model of male reproductive aging by administering d-gal injections to male mice and to determine the possible mechanism expediting senescence processes during spermatogenesis. In this study, C57Bl/6 mice were randomized into five groups (each containing 8–10 mice according to the daily intraperitoneal injection of vehicle control or 100 or 200 mg/kg dosages of d-gal for a period of six or eight weeks). First, mice subjected to d-gal injections for six or eight weeks demonstrated considerably decreased superoxide dismutase activity in the serum and testis lysates compared to those in the control group. The lipid peroxidation in testis also increased in the d-gal-injected groups. Furthermore, the d-gal-injected groups exhibited a decreased ratio of testis weight/body weight and sperm count compared to the control group. The percentages of both immotile sperm and abnormal sperm increased considerably in the d-gal-injected groups compared to those of the control group. To determine the genes influenced by the d-gal injection during murine spermatogenesis, a c-DNA microarray was conducted to compare testicular RNA samples between the treated groups and the control group. The d-gal-injected groups exhibited RNA transcripts of nine spermatogenesis-related genes (Cycl2, Hk1, Pltp, Utp3, Cabyr, Zpbp2, Speer2, Csnka2ip and Katnb1) that were up- or down-regulated by at least two-fold compared to the control group. Several of these genes are critical for forming sperm-head morphologies or maintaining nuclear integration (e.g., cylicin, basic protein of sperm head cytoskeleton 2 (Cylc2), casein kinase 2, alpha prime interacting protein (Csnka2ip) and katanin p80 (WD40-containing) subunit B1 (Katnb1)). These results indicate that d-gal-injected mice are suitable for investigating male reproductive aging.
   

  ✔本篇論文使用華聯產品:Mouse OneArray  
 Histochemistry And Cell Biology. doi: 10.1007/s00418-015-1348-9..
 Impact of diethylhexyl phthalate on gene expression and development of mammary glands of pregnant mouse.
 
 
 
  Abstract
The widely used diethylhexyl phthalate (DEHP) is a known endocrine disruptor that causes persistent alterations in the structure and function of female reproductive system, including ovaries, uterus and oviducts. To explore the molecular mechanism of the effect of DEHP on the development of mammary glands, we investigated the cell cycle, growth, proliferation and gene expression of mammary gland cells of pregnant mice exposed to DEHP. It was demonstrated, for the first time, that the mammary gland cells of pregnant mice treated with DEHP for 0.5–3.5 days post-coitum had increased proliferation, growth rate and number of cells in the G2/S phase. The expression of cell proliferation-related genes was significantly altered after short time and low-dose DEHP treatment of mammary gland cells in vivo and in vitro. These findings showed adverse effects of DEHP on mammary gland cells in pregnant mice.