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Source: Toxicology Letters

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Total 86 results found since Jan 2013.

The role of NAD(+)-dependent isocitrate dehydrogenase 3 subunit α in AFB1 induced liver lesion.
In this study, the sequences of IDH3α from various species were compared and the protein expression levels in different organs were examined, and the results showed that IDH3α was a widely distributed protein and shared highly conserved sequence in various species. In the same time, IDH3α was demonstrated to accumulate in a dose-dependent manner induced by AFB1 in cells, and was also up-regulated in the process of AFB1-induced liver lesion. Similar results were observed when H2O2 was used to replace AFB1. Over-expression of IDH3α increased the phosphorylation level of Akt (Protein kinase B) and neutralized the cellular...
Source: Toxicology Letters - November 5, 2013 Category: Toxicology Authors: Yang C, Fan J, Zhuang Z, Fang Y, Zhang Y, Wang S Tags: Toxicol Lett Source Type: research

Par-4 Downregulation Confers Cisplatin Resistance in Pancreatic Cancer Cells via PI3K/Akt Pathway-dependent EMT.
In conclusion, these results indicate that Par-4 downregulation confers CDDP resistance via PI3K/Akt pathway-dependent EMT in BXPC-3 cells. Therefore, Par-4 may be a potential target for overcoming CDDP resistance in pancreatic cancer. PMID: 24144893 [PubMed - as supplied by publisher]
Source: Toxicology Letters - October 18, 2013 Category: Toxicology Authors: Tan J, You Y, Xu T, Yu P, Wu D, Deng H, Zhang Y, Bie P Tags: Toxicol Lett Source Type: research

Mechanistic study on the biological effects of silver and gold nanoparticles in Caco-2 cells-induction of the Nrf2/HO-1 pathway by high concentrations of silver nanoparticles.
Abstract The most commonly used metal nanoparticles (NPs) across diverse applications, including in agro-food applications, include silver (AgNPs) and gold (AuNPs). In the present study, we aimed to investigate the biological responses and possible toxicological effects of AgNPs and AuNPs in the Caco-2 cells as an in vitro human GI tract model. Both AgNPs and AuNPs were internalized into the cytoplasm of Caco-2 cells, but not within the nucleus and only exposure to high concentrations of AgNPs, but not AuNPs, caused acute cytotoxicity and depolarization of the mitochondrial membrane potential. In addition, only Ag...
Source: Toxicology Letters - October 11, 2013 Category: Toxicology Authors: Aueviriyavit S, Phummiratch D, Maniratanachote R Tags: Toxicol Lett Source Type: research

Crotonaldehyde induces heat shock protein 72 expression that mediates anti-apoptotic effects in human endothelial cells.
Abstract Crotonaldehyde is a highly reactive aldehyde and a common environmental pollutant. It occurs in cigarette smoke and automobile exhaust, and is also endogenously generated by lipid peroxidation. Reactive aldehydes, such as crotonaldehyde, are considered to be important mediators of cell damage. Since endothelial apoptosis is considered to be the first step in the pathogenesis of cardiovascular disease, there have been many efforts to protect endothelial cell from oxidative stress. Heat shock protein 72 (HSP72) is a representative stress-inducible HSP70 family protein, and its synthesis is increased in resp...
Source: Toxicology Letters - September 23, 2013 Category: Toxicology Authors: Ryu DS, Yang H, Lee SE, Park CS, Jin YH, Park YS Tags: Toxicol Lett Source Type: research

Cadmium induces N-cadherin cleavage via ERK-mediated γ-secretase activation in C6 astroglia cells.
Abstract N-cadherin has known to be involved in tumor progression and metastasis. However, it is still obscure about the signaling pathway involving in the processing of N-cadherin. Thus, we examined which signaling pathway plays a major role in the processing of N-cadherin in C6 glioma cells following treatment of Cadmium (Cd), a highly ubiquitous heavy metal. A cleavage product of N-cadherin, N-cad/CTF2 was observed by the treatment of Cd to C6 cells in a time and concentration-dependent manner. The production of N-cad/CTF2 was inhibited by pretreatment of γ-secretase inhibitors or siRNA transfection of nicastr...
Source: Toxicology Letters - July 19, 2013 Category: Toxicology Authors: Jo C, Koh YH Tags: Toxicol Lett Source Type: research

MCM-2 is a therapeutic target of Trichostatin A in colon cancer cells.
Abstract Histone deacetylase (HDAC) inhibitors have recently emerged as a new class of anti-cancer agents. Trichostatin A (TSA), a classical HDAC inhibitor, has been demonstrated to induce cell cycle arrest, promote cell apoptosis, and inhibit metastasis. However, the molecular mechanism underlying TSA function has not been fully elucidated. In the current study, we found that TSA treatment induced altered expression of cell cycle-associated genes in HCT116 cells by RT-PCR array. Among the 84 genes related to cell cycle control, 34 genes were significantly altered by TSA treatment, with 7 genes upregulated and 27 ...
Source: Toxicology Letters - June 13, 2013 Category: Toxicology Authors: Liu Y, He G, Wang Y, Guan X, Pang X, Zhang B Tags: Toxicol Lett Source Type: research

Posttranslational mechanisms modulating the expression of the cytochrome P450 1A1 gene by methylmercury in HepG2 cells: A role of heme oxygenase-1.
In conclusion, this study demonstrated that MeHg inhibited the TCDD-mediated induction of CYP1A1 through a posttranslational mechanism and confirms the role of HO-1 in a MeHg-mediated effect. PMID: 23541843 [PubMed - in process]
Source: Toxicology Letters - May 22, 2013 Category: Toxicology Authors: Amara IE, Anwar-Mohamed A, El-Kadi AO Tags: Toxicol Lett Source Type: research

Cajaninstilbene acid (CSA) exerts cytoprotective effects against oxidative stress through the Nrf2-dependent antioxidant pathway.
This study examined the role of Nrf2 in CSA-mediated antioxidant effects on human hepatocarcinoma (HepG2) cell line. The generation of reactive oxygen species (ROS) upon H2O2 and CSA treatment was lower than that of H2O2 alone. CSA activated Nrf2 as evaluated by Western blotting. A luciferase reporter assay also demonstrated that CSA-activated signaling resulted in the increased transcriptional activity of Nrf2 through binding to the antioxidant response element (ARE) enhancer sequence. Our study indicated that treatment of HepG2 cells with CSA induces Nrf2-dependent ARE activity and gene expression of heme oxygenase-1 (HO...
Source: Toxicology Letters - May 22, 2013 Category: Toxicology Authors: Liang L, Luo M, Fu Y, Zu Y, Wang W, Gu C, Zhao C, Li C, Efferth T Tags: Toxicol Lett Source Type: research

Sanguinarine induces apoptosis in human colorectal cancer HCT-116 cells through ROS-mediated Egr-1 activation and mitochondrial dysfunction.
We examined the effects of sanguinarine, a benzophenanthridine alkaloid, on reactive oxygen species (ROS) production and the association of these effects with apoptotic cell death in a human colorectal cancer HCT-116 cell line. Sanguinarine generated ROS, which was followed by a decrease in the mitochondrial membrane potential (MMP), the activation of caspase-9 and -3, and the down-regulation of anti-apoptotic proteins, such as Bcl2, XIAP and cIAP-1. Sanguinarine also promoted the activation of caspase-8 and truncation of Bid (tBid). However, the quenching of ROS generation by N-acetyl-l-cysteine, a scavenger of ROS, rever...
Source: Toxicology Letters - May 6, 2013 Category: Toxicology Authors: Han MH, Kim GY, Yoo YH, Choi YH Tags: Toxicol Lett Source Type: research

Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts.
Abstract Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), yet pathogenic mechanisms are not fully understood. Vascular endothelial growth factor (VEGF) is one of the major regulators of endothelial cell survival and is believed to play a role in the pathogenesis of COPD. Fibroblasts are a significant source of VEGF in the lungs; however the effect of cigarette smoke exposure on VEGF release by fibroblasts is not fully understood. We hypothesized that cigarette smoke-induced disturbed VEGF release by human lung fibroblasts is a potential pathogenic mechanism that could contribute ...
Source: Toxicology Letters - April 22, 2013 Category: Toxicology Authors: Farid M, Kanaji N, Nakanishi M, Gunji Y, Michalski J, Iwasawa S, Ikari J, Wang X, Basma H, Nelson AJ, Liu X, Rennard SI Tags: Toxicol Lett Source Type: research

Paeoniflorin protects human EA.hy926 endothelial cells against gamma-radiation induced oxidative injury by activating the NF-E2-related factor 2/heme oxygenase-1 pathway.
This study was designed to confirm the protective effect of Paeoniflorin against radiation-induced endothelial cellular damage and to elucidate the underlying mechanisms. Preincubation of EA.hy926 cells with Paeoniflorin before γ-radiation resulted in significant inhibition of apoptosis, a decrease in mitochondrial membrane potential and enhanced cell viability. In particular, we showed that Paeoniflorin significantly reduced the formation of intracellular reactive oxygen species (ROS), the level of malondialdehyde (MDA) and lactate dehydrogenase (LDH) leakage, and enhanced production of the endogenous antioxidants, gluta...
Source: Toxicology Letters - February 8, 2013 Category: Toxicology Authors: Yu J, Zhu X, Qi X, Che J, Cao B Tags: Toxicol Lett Source Type: research