İşcan, Mümtaz

Ada, Ahmet Oğuz

Güler, Asena

Kunak, Celalettin Semih

Gülhan, Meral

Toxicology Letters

English

Ufuk Universitesi Akademik Acikerisim Sistemi

Abstracts / Toxicology Letters 280S (2017) S238–S242 S239toma (SH-SY5Y) cell line. IC50 value of AKB48 was calculated as160.91 M by MTT assay. Oxidative damage potential was evalu-ated by determining reactive oxygen species (ROS) production byflowcytometer, and glutathione (GSH) levels by ELISA kit. Treat-ment with higher concentrations of AKB48 induced ROS generation(≥1.2-fold); however GSH levels did not changed. Additionally,the regulations in cannabinoid receptors and inflammation-relatedgenes were determined on a qPCR platform. CB1 expression wasincreased approximately 15-fold at lower concentrations; whereasCB2 did not expressed. IL-6 and TNF- were up-regulated with adose-dependent manner, and the profiles were almost identical;however, MAPK8 and NF-B were slightly regulated.http://dx.doi.org/10.1016/j.toxlet.2017.07.660P-07-07-04Aryl hydrocarbon receptor is linked with novelfood avoidance behaviour in Sprague-DawleyratsSelma Mahiout, Jere Lindén, Ira Karppinen, Raimo PohjanvirtaUniversity of Helsinki, Helsinki, FinlandThe aryl hydrocarbon receptor (AHR) mediates the toxicity ofdioxins, but also plays important physiological roles. Previ-ously, below-toxic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxinand shorter-acting AHR agonists, including -naphthoflavone(BNF), were shown to induce strong avoidance of novel foods inrats. In contrast, 2,4,6-tryphenyldioxane-1,3, a phenobarbital-likeinducer that activates constitutive androstane receptor insteadof AHR, did not cause it. These results suggested dependence ofthe avoidance response specifically on AHR, a hypothesis testedhere. We used littermate AHR-knockout, heterozygote and wild-type Sprague-Dawley rats. Young adult male rats were habituatedto chocolate for ∼20 h before exposure to a single dose of BNF(60 mg/kg ig) or the vehicle. Subsequently, chocolate consump-tion was monitored for another 24 h. The AHR-phenotype of eachlineage was confirmed by quantifying hepatic Cyp1a1 mRNA, asensitive marker for AHR activation. Cyp1a1 was not found to beexpressed in AHR-knockouts or induced by BNF, contrary to theother two lineages. As hypothesised, BNF failed to influence choco-late intake in the knockouts; both groups consumed on average6.3–6.6 g by 24 h (p = 0.875). In contrast, in both the heterozygoteand wildtype lineages, BNF-treated rats exhibited strong chocolateavoidance, while the controls did not (respective 24-h consump-tions: 0.35 vs 5.1 g, p = 0.006; and 1.3 vs 8.3 g, p = 0.011). Thesefindings provide formal confirmation that AHR signalling is a pre-requisite for BNF-induced novel food avoidance behaviour.http://dx.doi.org/10.1016/j.toxlet.2017.07.661P-07-07-05CYP1B1*2 and CYP1B1*3 polymorphisms andclinical outcome in non-small cell lung cancerpatientsMumtaz Iscan 1, Ahmet Oguz Ada 1, Asena Guler 1, CelalettinSemih Kunak 2, Meral Gulhan 31 Department of Toxicology, Faculty of Pharmacy, Ankara University,Ankara, Turkey2 Department of Pharmacology, Faculty of Medicine, Ordu University,Ordu, Turkey3 Department of Chest Diseases, Ridvan Ege Hospital, Ufuk University,Ankara, TurkeyThe association between CYP1B1*2 and CYP1B1*3 polymorphismsand response to chemotherapy and survival of patients with non-small cell lung cancer (NSCLC) are limited and inconclusive. Inthis study, CYP1B1*2 and CYP1B1*3 polymorphisms and responseto platinum-based chemotherapy and survival in 137 advancedstage NSCLC patients were investigated. Genetic polymorphismanalyses were performed by conventional PCR and real time-PCR.The polymorphisms of CYP1B1*2 and CYP1B1*3 did not signifi-cantly influence the responses to chemotherapy and survival inNCSLC patients (p > 0.05). We also analysed these gene variantsin combination with CYP1A1*2C, CYP1B1*4, CYP2E1*5B, CYP2E1*6,CYP2E1*7B, GSTM1, GSTT1, GSTP1 exon 5, GSTP1 exon 6, GSTO1(A140D), and TP53 (Arg72Pro) polymorphic genes that we havepreviously genotyped in the same patients (Ada et al., Neoplasma,57, 512–527, 2010; Karacaoglan et al., Turk J Med Sci, 47, 554–562,2017). The multivariate analysis revealed that adjusted hazard ratio(HR) of death of the combined variant genotypes of CYP1B1*2 andCYP1A1*2C, and CYP1B1*2 and CYP1B1*4 increased significantly ascompared to wild-type genotypes (HR, 5.01; 95% CI, 1.52–16.19,p = 0.008, HR, 3.63; 95% CI, 1.12–11.78, p = 0.032, respectively).These results show that combined variant genotypes of CYP1B1*2and CYP1A1*2C, and CYP1B1*2 and CYP1B1*4 are associated withworsening of survival in NSCLC patients. (Supported by the grantsfrom Research Funds of Ankara University, nos: 15L0237003 and10A3336002.)http://dx.doi.org/10.1016/j.toxlet.2017.07.662P-07-07-06Dysregulated lncRNA-UCA1 contributes to theprogression of gastric cancer throughregulation of the PI3K-Akt-mTOR signalingpathwayChengyun Li, Geyu Liang, Jing Sui, Sheng Yang, Siyi XuKey Laboratory of Environmental Medicine Engineering, Ministry ofEducation, School of Public Health, Southeast University, Nanjing,ChinaThe long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been recently shown to be dysregulatedduring disease occurrence and to play an important role in theprogression of several cancers. However, the biological role andpotential regulation mechanism of UCA1 in the carcinogenesis ofgastric cancer remain unclear. In the present study, we found thatUCA1 was aberrantly upregulated in gastric cancer tissues andgastric cancer cell lines, and was associated with TNM stage andmetastasis. UCA1 silencing significantly inhibited gastric cancerBGC-823 cell proliferation and increased its apoptosis. We alsofound that UCA1 played an important role in the migration and

CYP1B1*2 and CYP1B1*3 polymorphisms andclinical outcome in non-small cell lung cancerpatients

http://acikerisim.ufuk.edu.tr/xmlui/bitstream/20.500.14065/1466/1/16-CYP1B12andCYP1B13polymorphisms%20andclinical%20outcome%20in%20non-small%20cell%20lung%20cancerpatients.pdf

CYP1B12 and CYP1B13 polymorphisms andclinical outcome in non-small cell lung cancerpatients

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