Veronika Tanhauserová

Brno University of Technology, Brünn, South Moravian, Czech Republic

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Publications (4)3.13 Total impact

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    ABSTRACT: Guinea pigs (Cavia porcellus) were treated with haloperidol (HP), and free radical (FR) and ferric reducing antioxidant power (FRAP) assays were used to determine oxidative stress levels. Furthermore, the superoxide dismutase (SOD), glutathione reductase (GR) and glutathione-S-transferase (GST) activity levels were detected and glucose levels and the reduced and oxidized glutathione (GSH/GSSG) ratio were measured in HP-treated and untreated guinea pigs. The present study demonstrated that the administration of HP causes significant oxidative stress in guinea pigs (P=0.022). In animals treated with HP, the activity of GST was significantly increased compared with a placebo (P= 0.007). The elevation of SOD and GR activity levels and increase in the levels of glutathione (GSH) in HP-treated animals were not statistically significant. In the HP-untreated animals, a significant positive correlation was observed between oxidative stress detected by the FR method and GST (r=0.88, P=0.008) and SOD (r=0.86, P= 0.01) activity levels, respectively. A significant negative correlation between the levels of plasma glucose and oxidative stress detected by the FRAP method was observed (r=-0.78, P=0.04). Notably, no significant correlations were observed in the treated animals. In the HP-treated group, two subgroups of animals were identified according to their responses to oxidative stress. The group with higher levels of plasma HP had higher enzyme activity and reactive oxygen species production compared with the group with lower plasma levels of HP. The greatest difference in activity (U/μl) between the two groups of animals was for GR.
    Experimental and therapeutic medicine 02/2013; 5(2):479-484. DOI:10.3892/etm.2012.822 · 0.94 Impact Factor
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    ABSTRACT: Several typical characteristics of prostate tissue have been identified including the ability to accumulate zinc(II). However, this feature of prostate cells is lost during carcinogenesis and, thus, prostate cells are unable to accumulate zinc(II) ions in high levels. Therefore, we can expect that zinc(II) ions can significantly contribute to the progression of tumour disease and to the ability of prostate cell lines to metastasize. In this study, we aimed our attention on determining the expression of Bcl-2, c-Fos, c-Jun, Ki-67, NF-κB and p53 genes in two prostate cell lines, as the 22Rv1 cell line, a model of aggressive partially androgen-sensitive prostate cancer and the PNT1A cell line, a normal prostate cell line model. Moreover, we were interested in the mechanisms through which exposure of these cell lines to zinc(II) ions could influence expression of the above-mentioned genes. We found that zinc(II) ions caused elevated expression of Ki-67, a marker of proliferation, extremely low expression of p53, high expression of Bcl-2 and no changes in the expression of p53. Our experimental data show different effect of zinc(II) ions on expression of the above-mentioned regulatory genes, which may give us more information on their impact on cancer development and progression with possible using for cancer therapy.
    Oncology Reports 07/2012; 28(3):806-14. DOI:10.3892/or.2012.1897 · 2.19 Impact Factor
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    ABSTRACT: Úvod: Patologická aktivace systému renin-angiotenzin-aldosteron (RAAS) je důležitým patogenetickýcm mechanizmem vzniku a progrese diabetické nefropatie (DN). Geny kódující složky RAAS jsou polymorfní, některé z variant mohou ovlivňovat odpověď na léčbu blokátory RAAS. Cílem projektu bylo zjistit, jakým způsobem modifikují vybrané varianty genů efekt léčby a progresi renálního postižení u diabetiků 2. typu (T2DM). Metodiky: Do průřezové studie bylo zařazeno 321 osob s T2DM s variabliním postižením ledvin (normo- a mikroalbuminurie, proteinurie a ESRD, prům. věk 67 let, 160 mužů a 161 žen), které byly pravidelně sledovány po dobu 37 měsíců [21-58] (medián, [IQR]). Pomocí PCR jsme z DNA detekovali 8 jednonukleotidových polymorfizmů (I/D ACE, ATG M235T, ATR1 A1166C, CYP11B2 -344T/C, HSD11B1 83557insA, HSD11B2 G534A, MR G3514C, MR A4582C). Sledovali jsme následující klinické end-points: (1) progrese DN definovaná jako dosažení vyššího stadia DN za dobu sledování, (2) závažná kardiovaskulární událost (MCVE), a (3) celková mortalita (ACM). K odhadu rizika sledovaných end-points jsme použili Coxův regresní model a k odhadu incidence Kaplan-Meirovu analýzu s log-rank testem. Pro účely farmakogenetické studie jsme sledovali léčbu inhibitory angiotenzin konvertujícího enzymu (ACEi) a blokátory receptoru AT1 (sartany). Kumulativní dávka podávané účinné látky za celou dobu sledování byla přepočtena u ACEi na jednotky captoprilu, u sartanů na jednotky losartanu. Výsledky: Ze sledovaných end-points jsme nalezli statisticky významný rozdíl u celkové mortality mezi skupinami rozdělenými podle genotypů polymorfizmu A4582C v genu pro mineralokortikoidní receptor (P = 0,007; log-rank test). Detailní farmakogenetické analýzy celého souboru probíhají a budou k dispozici v době konání konference. Závěr: Protože farmakologická blokáda RAAS ovlivňuje základní patogenetický systém vzniku DN, jistý genetický efekt na farmakoterapii je nutno brát v úvahu. Výstupem studia by mohla být větší aplikace personalizované medicíny do léčby DN. Poděkování: Práce byla podpořena grantem MZ ČR NT11405.
    48. Diabetologické dny 2012, Luhačovice, Czech Republic; 04/2012
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    ABSTRACT: Diabetic nephropathy (DN) is one of the most common and serious complications of diabetes mellitus with pathological activation of renin-angiotensin-aldosterone system (RAAS) as the key pathogenetic mechanism. Pharmacological blockade of RAAS represents the main renoprotective treatment of DN. Several single nucleotide polymorphisms (SNPs) were shown to influence interindividual variability of RAAS (e.g circulating levels of RAAS compounds and enzyme activities). These functional genetic variants are supposed to modify therapeutic effect of RAAS blockers. Genetic variability together with other factors, which are objects of therapeutical compensation (e.g. glycaemia, blood pressure, proteinuria, lipidaemia and body weight) can affect progression of kidney damage in diabetics. The aim of this project is to study the effect of genetic variability in the selected components of RAAS in the progression of kidney disease by diabetic patients. Three SNPs in angiotensin converting enzyme (ACE - rs4343), angiotensinogen (ATG M235T - rs699) and angiotensin II type I receptor gene (ATR1 A1166C - rs5186) were genotyped using restriction fragment length polymorphism PCR. This case – case study involved 433 patients with a different degree of DN. Results of the haplotype analysis will be compared with a pharmacological treatment - especially RAAS blockers. We expect a variability of haplotypes in RAAS genes among patients with different degree of DN and a possibility of an implementation of phamacogenomic approach to the treatment of DN. This study was supported by the project IGA NT11405-6.
    XV. setkání biochemiků a molekulárních biologů, Brno, Czech Republic; 11/2011

Publication Stats

9 Citations
3.13 Total Impact Points

Institutions

  • 2013
    • Brno University of Technology
      • Department of Microelectronics
      Brünn, South Moravian, Czech Republic
  • 2012
    • Masaryk University
      Brünn, South Moravian, Czech Republic