Dana Kotyzová

Charles University

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V. Eybl

Charles University

J. Koutenský

Charles University

PČ

Pavla Černá

Colorado State University

Anna Hodková

Charles University

Monika Bludovská

Charles University

Eystein Glattre

Norwegian University of Life Sciences

Július Brtko

Institute of Experimental Endocrinology of the Slovak Academy of Sciences

Eybl

Charles University

Věra Míčková

Charles University

L. Lešetický

Charles University

Cooperative Institutions

Charles University

Vanderbilt University

Institute of Experimental Endocrinology of the Slovak Academy of Sciences

University Hospital Plzen

Slovak Academy of Sciences

Purdue University West Lafayette

Institute of Endocrinology

Sharda University

University of West Bohemia

Institute of Electrical Engineering of the Slovak Academy of Sciences

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Impact of thioacetamide induced hepatic cirrhosis on sympathetic innervation of the rat heart

Autonomic Neuroscience (2013)

Eliška Mistrová Monika Bludovská Dana Kotyzová Jana Slavı́ková Markéta Dvořáková

Sympathetic nervous system

Hyperdynamic circulation

Thioacetamide

10.1016/j.autneu.2013.05.120

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The influence of deferiprone (L1) and deferoxamine on iron and essential element tissue level and parameters of oxidative status in dietary iron-loaded mice

Toxicology Letters (2002)

V. Eybl Dana Kotyzová Metodı̀j Kolek J. Koutenský Peter Nielsen

Deferiprone

10.1016/s0378-4274(01)00541-0

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Citations (32)

The influence of curcumin and manganese complex of curcumin on cadmium-induced oxidative damage and trace elements status in tissues of mice

Journal of Applied Toxicology (2005)

V. Eybl Dana Kotyzová L. Lešetický Monika Bludovská J. Koutenský

Curcumin (diferuoyl methane) from turmeric is a well-known biologically active compound. It has been shown to ameliorate oxidative stress and it is considered to be a potent cancer chemopreventive agent. In our previous study the antioxidative effects of curcumin in cadmium exposed animals were demonstrated. Also manganese exerts protective effects in experimental cadmium intoxication. The present study examined the ability of the manganese complex of curcumin (Mn-curcumin) and curcumin to protect against oxidative damage and changes in trace element status in cadmium-intoxicated male mice. Curcumin or Mn-curcumin were administered at equimolar doses (0.14 mmol/kg b.w.) for 3 days, by gastric gavages, dispersed in methylcellulose. One hour after the last dose of antioxidants, cadmium chloride (33 µmol/kg) was administered subcutaneously. Both curcumin and Mn-curcumin prevented the increase of hepatic lipid peroxidation — expressed as MDA level, induced by cadmium intoxication and attenuated the Cd-induced decrease of hepatic GSH level. No change in hepatic glutathione peroxidase or catalase activities was found in Cd-exposed mice. A decreased GSH-Px activity was measured in curcumin and Mn-curcumin alone treated mice. Neither curcumin nor Mn-curcumin treatment influenced cadmium distribution in the tissues and did not correct the changes in the balance of essential elements caused by Cd-treatment. The treatment with Mn-curcumin increased the Fe and Mn content in the kidneys of both control and Cd-treated mice and Fe and Cu content in the brain of control mice. In conclusion, regarding the antioxidative action, introducing manganese into the curcumin molecule does not potentiate the studied effects of curcumin. Copyright © 2005 John Wiley & Sons, Ltd.

TRACE (psycholinguistics)

10.1002/jat.1124

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Citations (61)

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat

Biomedical Papers (2005)

Dana Kotyzová V. Eybl Martin Mihaljevič Eystein Glattre

The aim of this study was to evaluate the influence of arsenic and bromine exposure with or without iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A - standard diet, group B - iodine rich diet (10 mg I/kg food), group C - selenium rich diet (1 mg Se/kg) and group D - iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO(2) ip (6.5 mg.kg(-1) twice a week for two weeks and 3.25 mg.kg(-1) for six weeks) or KBr in drinking water (58.8 mg.l(-1)) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland ( approximately 18 ppm of As, approximately 90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to approximately 50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.

10.5507/bp.2005.052

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Citations (16)

Toxicity and adverse effacts of cholestore

Toxicology Letters (1995)

V. Eybl Dana Kotyzová D. Caisová J. Koutenský Katrina Blazek

10.1016/0378-4274(95)94619-r

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506 Protective effect of IP administered olive oil in acute cadmium intoxication

Toxicology Letters (2003)

V. Eybl Dana Kotyzová J. Koutenský

CADMIUM EXPOSURE

10.1016/s0378-4274(03)90505-4

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Expression of classical mediators in hearts of rats with hepatic dysfunction

Canadian Journal of Physiology and Pharmacology (2017)

Dagmar Jarkovská Monika Bludovská Eliška Mistrová Věra Křížková Dana Kotyzová

Liver cirrhosis is associated with impairment of cardiovascular function including alterations of the heart innervation, humoral and nervous dysregulation, changes in systemic circulation and electrophysiological abnormalities. Choline acetyltransferase (ChAT), enzyme forming acetylcholine, tyrosine hydroxylase (TH), and dopamine-β-hydroxylase (DBH), enzymes participating in noradrenaline synthesis, are responsible for the production of classical neurotransmitters, and atrial natriuretic peptide (ANP) is produced by cardiomyocytes. The aim of this study was to evaluate the influence of experimentally induced hepatic dysfunction on the expression of proANP, ChAT, TH, and DBH in the heart. Hepatic dysfunction was induced by application of thioacetamide (TAA) or by ligation of bile duct. Biochemical parameters of hepatic injury and levels of peroxidation in the liver and heart were measured. Liver enzymes measured in the plasma were significantly elevated. Cardiac level of peroxidation was increased in operated but not TAA group animals. In the left atrium of operated rats, the expression of TH and DBH was lower, while expression of ChAT remained unchanged. In TAA group, no significant differences in the expression of the genes compared to controls were observed. Liver injury induced by ligation leads to an imbalance in the intracardiac innervation, which might impair nervous control of the heart.

10.1139/cjpp-2017-0060

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Citations (6)

Role of astrocytes in trimethyltin neurotoxicity

Journal of Biochemical and Molecular Toxicology (2001)

Palur G. Gunasekar Vera Mickova Dana Kotyzová Li Li Joseph L. Borowitz

Although the neurotoxicity of trimethyltin (TMT) is well known, mechanisms are still not clear. Glia have been proposed to mediate the toxic action of TMT on nerve cells. Accordingly, the effects of TMT were tested in primary neuronal cultures from rat cerebellum and compared to effects in astrocytes and mixed cultures. Neuronal damage observed following TMT exposure was less in the presence of astrocytes and astrocytes alone were resistant to TMT. Thus, astrocytes have a protective effect against TMT-induced neurotoxicity. TMT caused an oxidative stress in granule cell cultures involving a variety of oxidative species (O2)*-, H2O2, NO), but astrocytes were less sensitive to TMT-induced oxidative species generation. Antioxidants, glutathione and 7-nitroindazole attenuated neuronal cell death induced by TMT. It appears that oxidative stress mediates a large part of the destructive action of TMT in neuronal cultures. The presence of astrocytes appears to modulate TMT-induced oxidative stress so that TMT causes only a small increase in lipid peroxidation in mouse brain after systemic administration. Thus, TMT induces a pronounced oxidative stress in cultured neurons, but when astrocytes are present, oxidative species play a lesser role in the neurotoxic action of TMT.

Neurotoxicity

Neuroglia

10.1002/jbt.10004

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Citations (40)

Interaction of captopril with iron(III)—Effect on oxidative stress and mineral status in rats

Toxicology Letters (2010)

V. Eybl Dana Kotyzová Anna Hodková

Captopril

10.1016/j.toxlet.2010.03.950

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