Vesile Duzguner | Ardahan University (original) (raw)

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Papers by Vesile Duzguner

Pakistan Journal of Zoology, 2013

Oriental Journal of Chemistry, 2015

Pesticide Biochemistry and Physiology, 2012

Imidacloprid is the most important example of the neonicotinoid insecticides known to target the ... more Imidacloprid is the most important example of the neonicotinoid insecticides known to target the nicotinic acetylcholine receptor (nAChR) in insects, and potentially in mammals. In the present study, oxidant and inflammatory responses to chronic exposure of imidacloprid was studied in rats. Wistar rats were randomly allocated into two groups as control and imidacloprid-exposed group (n = 10 rat/each group). 1 mg/kg/BW/day imidacloprid was administrated orally by gavage for 30 days. After exposure, rats were euthanized and liver and brain samples were surgically removed for analyses. Imidacloprid application caused a significant increase in nitric oxide production in brain (p < 0.05) and liver (p < 0.001). The quantitative analyses of mRNA confirmed the finding that imidacloprid induced the mRNA transcriptions of the three isoforms of nitric oxide synthases (iNOS, eNOS, nNOS) in brain and two isoforms (iNOS, eNOS) in the liver. Exposure to imidacloprid caused significant lipid peroxidation in plasma, brain (p < 0.001) and liver (p < 0.003). While the superoxide-generating enzyme xanthine oxidase activity was elevated in both tissues (p < 0.001), myeloperoxidase activity was increased only in the liver (p < 0.001). Antioxidant enzyme activities showed various alterations following exposure, but a significantly depleted antioxidant glutathione level was detected in brain (p < 0.008). Evidence of chronic inflammation by imidacloprid was observed as induction of pro-inflammatory cytokines such as TNF-a, IL-1b, IL-6, IL-12 and IFN-c in the liver and brain. In conclusion, chronic imidacloprid exposure causes oxidative stress and inflammation by altering antioxidant systems and inducing pro-inflammatory cytokine production in the liver and central nervous system of non-target organisms.

Research in Veterinary Science, 2010

Brucella species are able to survive and replicate within the phagocytic cells and cause chronic ... more Brucella species are able to survive and replicate within the phagocytic cells and cause chronic infections in domestic animals and humans. Modulation of programmed cell death by Brucella spp. may be one of the reasons of the chronicity of the infection. In this study, whether cisplatin treatment, an apoptotic anticancer agent, would enhance the host resistance against Brucella melitensis-infected human macrophagelike cells was investigated. The infection neither induced inflammation nor oxidative stress. But, Brucella caused a decrease in infected macrophage viability of 36% at 48 h postinfection (p.i.) as compared with uninfected cells. Treatment of infected macrophages with 20 lM cisplatin for 48 h caused a large increase in nitric oxide (NO) levels in a time-dependent manner via induction of iNOS transcription. Cisplatin also enhanced glutathione peroxidase, myeloperoxidase and xanthine oxidase activities, providing evidence of generation of reactive free radicals. N-acetylcysteine was able to decrease cisplatin-induced NO, and prevented the agent-induced apoptosis, similar to effects found in L-NAME (N(G)-nitro-L-arginine methyl ester) treatment. Cisplatin stimulated inflammation through the induction of TNF-a and IL-12 secretion, and down-regulated Brucella-stimulated IL-10 transcription. The number of infected cells and their viability were decreased by 80% at 48 h p.i. by cisplatin in comparison with infected cells. Similar to this result, cisplatin treatment resulted in reduced intracellular CFU of B. melitensis being reduced by 80% at 48 h p.i. These findings demonstrate that pharmacological agents such as cisplatin may be considered to influence immune responses and apoptosis to help decrease Brucella-infected cell number.

Research in Veterinary Science, 2013

Cellular prion proteins (PrP C ) are mainly expressed in the central nervous system where they ha... more Cellular prion proteins (PrP C ) are mainly expressed in the central nervous system where they have antioxidant effects and a role in the endocytosis of bacteria within cells. These proteins also have some crucial biological functions including roles in neurotransmission, signal transduction and programmed cell death. However, the role of prion proteins in neuronal Brucella infection, specifically in the interaction of the pathogen and the host cell is controversial. In the present study, the silencing of PrP C mRNA by small interfering RNA (siRNA) transfection was investigated in human microglia cells infected with Brucella melitensis. More than 70% of prion proteins were down-regulated in microglia by siRNA transfection and this caused a slight decrease in the cellular viability of the control cells. Silencing of PrP C suppressed the antioxidant systems, though it led to an up-regulation of pro-inflammatory cytokines such as IL-12 and TNF-a as demonstrated by qRT-PCR analysis. B. melitensis infection of prion protein-silenced cells led to increase host viability, but had no effect on bacterial phagocytosis. According to the present study, there is no significant effect of prion proteins on phagocytosis and intracellular killing of B. melitensis in microglia cells.

Pesticide Biochemistry and Physiology, 2010

Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet ... more Imidacloprid is a neonicotinoid insecticide and has been extensively used as a crop pest and pet flea control programme because it's high specificity as an insecticide. Imidacloprid toxicity on mammalian tissues has not been adequately evaluated. In the present study, potential acute neuro and liver toxic effects of imidacloprid were analyzed in rats as a model of mammalian using antioxidant-oxidant and inflammatory system. 10 lM imidacloprid was administrated intravenously and 2 h post-administration, the rats were sacrificed, liver and brains were surgically removed. Exposure to imidacloprid led to significant increases in nitric oxide concentrations in brain, liver and plasma samples. The quantitative mRNA transcriptional analyses demonstrated that imidacloprid-elevated production of NO levels due to the induction of iNOS in liver, but neither nNOS nor iNOS were induced in brain. The oxidant-generating enzymes xanthine oxidase and myeloperoxidase activities in both tissues were elevated and significant lipid peroxidation in liver and plasma was observed. The antioxidant catalase, superoxide dismutase and glutathione peroxidase activities were differently responded to imidacloprid administration. Significant intracellular glutathione depletion was also measured in both tissues. Imidacloprid treatment upregulated inflammatory cytokines TNF-a, IL-6 and IL-1b mRNA transcriptions by 2.5-to 5.2-fold increases in both brain and liver. Conversely, anti-inflammatory mediator IL-10 mRNA was down-regulated in both organs. These results suggest that imidacloprid cause oxidative stress and inflammation in central nervous system and liver in non-target organisms in rats.

Journal of Applied Animal Research, 2008

Duzguner, V., Kucukgul, A., Erdogan, S., Celik, S. and Sahin, K. 2008. Effect of lycopene adminis... more Duzguner, V., Kucukgul, A., Erdogan, S., Celik, S. and Sahin, K. 2008. Effect of lycopene administration on plasma glucose, oxidative stress and body weight in streptozotocin diabetic rats. J. Appl. Anim. Res., 33: 17-20.

Free Radical Biology and Medicine, 2007

The effects of oral zinc supplementation on lipid peroxidation and the antioxidant defense system... more The effects of oral zinc supplementation on lipid peroxidation and the antioxidant defense system of alloxan (80-90 mg/kg)-induced diabetic rabbits were examined. Forty-five New Zealand male rabbits, 1 year old, weighing approximately 2.5 kg, were allocated randomly and equally as control, diabetic, and zinc-supplemented diabetic groups. After diabetes was induced, zinc-supplemented diabetic rabbits had 150 mg/L of zinc as zinc sulfate (ZnSO(4)) in their drinking tap water for 3 months. The feed and water consumption was higher in diabetic groups than (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01) healthy rabbits. The body weight was lower in diabetic rabbits compared to control. The blood glucose levels were higher in diabetic groups than controls. The elevated plasma malondialdehyde (MDA) levels were determined in the diabetic group (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01). The glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and ceruloplasmin levels in the diabetic group were decreased by the effect of diabetes but there was no difference between zinc-supplemented diabetic and control rabbits. Serum zinc concentrations were lower in diabetic rabbits but iron (Fe) and copper (Cu) levels in sera were not different among the groups. As a result, it was concluded that daily zinc supplementation could reduce the harmful effects of oxidative stress in diabetics.

Brucella species can settle and proliferate in microglial cells of host animals. The primary focu... more Brucella species can settle and proliferate in microglial cells of host animals. The primary focus of this mini-review is to discuss the biochemical and pathogenic processes that could potentially develop be-tween the host and the agent. Brucella's antioxidant responses to host's oxidative reactions, which are one of the defense systems in neuronal cells against the Brucella infection, are believed to be an important element in its pathogenicity; however their exact mechanisms to exert pathogenicity are not fully under-stood. In this review, the effects of cellular prion proteins (PrP C) on entrance of Brucella into host cells and on development of oxidative defenses in the host cells will be discussed. Additionally, we will discuss the potential of utilizing small interference RNA or short interference RNA to suppress the expression of PrP C and determine the subsequent effect on Brucella infection on microglial cells. Finally the effects of PrP C on oxidative events, and r...