Wyniki wyszukiwania

1

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

100%

Sun X., Liu Y., Hu G., Wang H.

Cellular and Molecular Biology Letters

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2004

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tom 09

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nr 3

This study aimed to assess whether nicotine prevented glutamate neurotoxicity in PC12 cells, and to identify the molecular mechanisms of any effects. The results showed that glutamate neurotoxicity in PC12 cells could be prevented by treatment with nicotine at concentrations of 10 nmol.l-1-1 mmol.l-1. This effect was in turn found to be inhibited by the application of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine. Nicotine significantly decreased the basal level of intracellular free Ca2+ and enhanced the buffering action on Ca2+ overload induced by high concentrations of glutamate (5 mmol.l-1). In addition, nicotine treatment up-regulated the mRNA and protein expression of apoptosis-related factors including bcl-2 mRNA and protein, but down-regulated the expression of bax mRNA and protein. It is concluded that the protective effects of nicotine against the neurotoxicity induced by glutamate are mediated by nAChRs, due to the increased buffering action on Ca2+ and the modulation of apoptotic processes.

2

The third neurotoxicity caused by organophosphorous pesticides

86%

Kinebuchi H., Shiraishi N., Konishi Y.

Annals of Agricultural and Environmental Medicine

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1994

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tom 01

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nr 2

3

Rat sciatic nerve lysosomal enzyme activity as a test for noncholinergic neurotoxic effect of Bromphenvinphos

86%

Biel-Zielinska A., Gradowska-Olszewska I., Brzezinski J., Piesko T., Zajac A., Goldnik A.

Acta Poloniae Toxicologica

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1995

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tom 03

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nr 1

4

Effects of repeated systemic penicillin injections on nonconvulsive and convulsive epileptic seizures in the rat

86%

Stankiewicz J., Stankiewicz M., Wiaderna-Stepien D., Tomas T., Gralewicz S.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 4

5

The evaluation of the role of mGluR7 in neuronal apoptotic processes by usage of AMN082, a selective mGluR7 agonist and mGluR7 knockout-derived cells

72%

Jantas D., Lech T., Pilc A., Lason W.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

Increasing body of evidence suggests a neuroprotective potential of metabotropic glutamatergic receptor group III (mGluR III) stimulation, however the role of particular subtypes of these receptors (mGluR4, mGluR7, mGluR8) in apoptotic processes is not fully recognized. Of special interest is the study on the role of mGluR7 which is widely expressed throughout the brain and recently developed selective positive allosteric modulator of this receptor, AMN082 (N,N=-dibenzhydrylethane-1,2-diamine dihydrochloride) enables investigation the biological role of mGluR7. In the present study, firstly we evaluated the possible neuroprotective effects of AMN082 (0.001–1 µM) on neurotoxicity induced by various apoptotic [stimuli staurosporine (St), doxorubicin (Dox) and low potassium (LP)] in 7 DIV cerebellar granule cells (CGC). The data showed that AMN082 (0.1–1 µM) partially attenuated the cell death induced by St and LP, but not by Dox. Next, we investigated the role of mGluR7 in neuronal cell death by testing the vulnerability of CGC from wild and mGluR7KO animals to toxic action of St, Dox and LP. No differences between groups under basal conditions have been found. However, after primary deprivation of CGC cells from potassium in culture medium and secondary application of proapoptotic stimuli we observed the higher vulnerability of mGluR7KO CGC to cell damaging effect of St and Dox but not LP. Further experiments performed on cortical glia cells demonstrated higher toxic action of St and Dox in mGluR7KO cells when compared to wild type one. Additionally, in mGluR7KO glia cells we found higher basal and stimulated by St or Dox caspase-3 activity when compared to wild type one. The obtained data suggest that specific stimulation of mGluR7 by AMN082 could be protective against staurosporine and low-potassium induced neuronal ell death. Moreover, the presence of mGluR7 could be particularly important for survival of glia cells under harmful conditions. The study was supported by statutory funds for Institute of Pharmacology PAS and grant No NN405611638 from the Ministry of Science and Higher Education, Warsaw, Poland.

6

Repeated isoflurane exposures of neonatal rats contribute to cognitive dysfunction in juvenile animals: the role of miR-497 in isoflurane-induced neurotoxicity

72%

Que Y., Zhang F., Peng J., Zhang Z., Zhang D., He M.

Folia Histochemica et Cytobiologica

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2021

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tom 59

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nr 2

7

Non-Abeta component of Alzheimer's disease amyloid and amyloid beta peptides evoked poly(ADP-ribose) polymerase-dependent release of apoptosis-inducing factor from rat brain mitochondria

72%

Adamczyk A., Czapski G. A., Jesko H., Strosznajder R. P.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 2

5-13

Amyloid beta peptide (Aß) and non-Aß component of Alzheimer’s disease amyloid (NAC) are involved in pathomechanism of Alzheimer's Disease (AD) and are deposited in the AD brain in the form of senile plaques. However, the mechanism of their neurotoxicity is not fully understood. In this study the sequence of events involved in NAC and Aß peptides evoked toxicity was investigated in brain slices, synaptosomes and in subcellular fractions. Radio-, immunochemical, spectrophotometrical methods and DNA electrophoresis were used in this study. Our data indicated that Aß 1-40 (25 µM) and NAC (10 µM) peptides induced liberation of free radicals and massive DNA damage that lead to activation of DNA bound enzyme poly(ADP-ribose) polymerase-1 (PARP-1). In consequence of these processes apoptosis-inducing factor (AIF) was released from mitochondria and was translocated to nucleus. The inhibitor of PARP, 3-aminobenzamide significantly decreased AIF release from mitochondria and its translocation. Both peptides under the investigated conditions had no effect on caspase-3 activity. Our data indicated that Aß and NAC peptides stimulate AIF-dependent apoptotic pathway that seems to be caspase independent process. The inhibition of PARP-1 may protect the brain against Aß and NAC toxicity.

8

Effects of p53 inhibitor on survival and death of cells subjected to oxidative stress

72%

Strosznajder R. P., Jesko H., Banasik M., Tanaka S.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

|

nr 4

215-221

Our previous data indicate that ischemia and amyloid beta peptide (Abeta) cause an oxidative damage to macromolecules. In the present study we investigated the role of p53 protein in cell survival and death after administration of Abeta. The experiments were carried out on pheochromocytoma cells (PC-12) and cortical primary neurons in culture. The cortical neurons were exposed (48 h, 10 µM) to the action of a short Abeta25-35 neurotoxic fragment and the involvement of p53 was evaluated after addition of the p53 inhibitor pifithrin-alpha. Changes in cell morphology were evaluated by 4', 6-diamidino-2-phenylindole staining and the concentration-dependent effect of pifithrin-alpha on cells viability was determined. Additionally, we studied the effect of pifithrin-alpha on neuronal survival in vivo after a 5-min global brain ischemia followed by 7 days' reperfusion in gerbils. We found that Abeta enhanced apoptotic cell death in cortical primary neurons. Pifithrin-alpha, at a 10 µM final concentration, protected the neuronal cells from the apoptotic death. However, at concentrations of 0.1 and 1 mM, the p53 inhibitor decreased PC-12 cells' viability in a dose-dependent manner. In in vivo experiments we did not observe any neuroprotection by pifithrin-alpha in the CA1 hippocampal layer, which suggests that its effects strongly depend on the duration and type of an ischemic insult. Our data indicate that pifithrin-alpha affects neuronal cells in a dual manner. It has a protective effect at a low concentration, but becomes neurotoxic at higher concentrations.

9

Assessment of neurotoxicity of pharmacological compounds during early neural development of human embryonic stem cells

72%

Kang H. Y., Hong E. J., Kang H. S., Ahn C., Jeung E. B.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 2

10

Essentiality and toxicity of vanadium supplements in health and pathology

72%

Gruzewska K., Michno A., Pawelczyk T., Bielarczyk H.

Journal of Physiology and Pharmacology

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2014

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tom 65

|

nr 5

11

Acute cytotoxicity evoked by tetrabromobisphenol A in primary cultures of rat cerebellar granule cells outweighs the effects of polychlorinated biphenyls

72%

Zieminska E., Stafiej A., Toczylowska B., Lazarewicz J. W.

Polish Journal of Environmental Studies

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2012

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tom 21

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nr 4

The aim of this study was to identify, among selected environmental toxins, the substance with the highest in vitro toxicity to neurons combined with the most marked induction of calcium imbalance, oxidative stress and mitochondrial dysfunction. Exposure of primary cultures of rat cerebellar granule cells for 30 min to polychlorinated biphenyls (PCBs) or brominated flame retardants (BFRs) at concentrations of 10-50 µM identified tetrabromobisphenol A as the compound with the highest toxicity. At a concentration of 25 µM, apart from the moderate activation of ⁴⁵Ca uptake, this BFR induced the most pronounced increase in intracellular Ca²⁺ concentration, depolarization of mitochondria, and activation of ROS production.

12

Causes of L-cysteine neurotoxicity

72%

Wlodek L.

Acta Biologica Cracoviensia. Series Zoologia

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2002

|

tom 44

13

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The role of nitric oxide in paraquat-induced oxidative stress in rat striatum

72%

Djukic M., Jovanovic M. C., Ninkovic M., Vasiljevic I., Jovanovic M.

Annals of Agricultural and Environmental Medicine

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2007

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tom 14

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nr 2

The role of nitric oxide (NO) in paraquat (PQ)-induced neurotoxicity is still not fully understood. In this study we used NG-nitro-L-arginine methyl ester (L-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, in order to examine the effects of NO, reactive oxygen species (ROS) generation and lipid peroxidation (LPO) development during PQ-mediated neurotoxicity. Oxidative stress development in the striatum of Wistar rats intrastriatally (i.s.) poisoned with PQ (and in some cases pre-treated with L-NAME) was investigated by measuring superoxide anion (O2 •ˉ), malondialdehyde (MDA) and nitrate (NO3ˉ), 30 min, 24 hours and 7 days after treatment. L-NAME pretreatment provided the possibility to distinguish the role of ROS from reactive nitrogen species (RNS) in oxidative stress development induced by PQ. Our results confi rm the involvement of NO in PQ-mediated neurotoxicity and reduced LPO by L-NAME pretreatment implying that the latter has a protective role.

14

How does trimethyltin affect the brain: facts and hypotheses

72%

Koczyk D.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

|

nr 2

15

Effects of 17-beta estradiol and estriol on NMDA-induced toxicity and apoptosis in primary cultures of rat cortical neurons

72%

Kajta M., Budziszewska B., Marszal M., Lason W.

Journal of Physiology and Pharmacology

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2001

|

tom 52

|

nr 3

16

Calcium transients in brain ischemia : role in neuronal injury

72%

Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

|

nr 1

17

The influence of repeated systemic penicillin injections at subconvulsive doses on spontaneous Spike-Wave Discharges in the rat

72%

Stankiewicz J., Gralewicz S.

Acta Neurobiologiae Experimentalis

|

1996

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tom 56

|

nr 3

18

The effects of organic solvents on poly[ADP-ribose] polymerase-1 activity: implications for neurotoxicity

72%

Banasik M., Stedeford T., Strosznajder R. P., Persad A. S., Tanaka S., Ueda K.

Acta Neurobiologiae Experimentalis

|

2004

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tom 64

|

nr 4

19

Effect of bifenthrin on memory processes, movement activity, and coordination in mice exposed to transient cerebral oligaemia

72%

Nieradko-Iwanicka B., Borzecki A.

Bulletin of the Veterinary Institute in Puławy

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2008

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tom 52

|

nr 2

The purpose of the present study was to examine whether the effects of exposure to 0.1LD₅₀ of bifenthrin on memory processes, movement activity, and coordination could be exacerbated by transient reduction of cerebral oxygen supply. The transient occlusion of both common carotid arteries (BCCA) in adult mice was performed under anaesthesia. Intraperitoneal LD₅₀ for bifethrin was estimated to be 16.1mg/kg b.w. The memory retention was evaluated in a step-through passive avoidance task (PA), working spatial memory in a Y-maze, movement coordination on a rota-rod, and movement activity in an automated device. Long-term memory impairment caused by bifenthrin was exacerbated by BCCA. Movement co-ordination was significantly altered in animals treated with the compound. Movement activity was slightly decreased in animals after BCCA and pesticide injection. These results indicate that cerebral oligaemic hypoxia potentiates long-term memory impairing effect of bifenthrin.

20

Is the NMDA receptor involved in neurotoxicity of pvp-coated silver nanoparticles? Study on primary cultures of cerebellar granule cells

58%

Zieminska E., Stafiej A., Struzynska L.

Acta Neurobiologiae Experimentalis

|

2013

|

tom 73

|

nr 1

Silver nanoparticles (NAg) possess antibacterial properties thus are widely used in many applications in medicine, life sciences and biotechnology. Nanoparticles can be found in vertebrate brain, but little is known about their neurotoxicity. The aim of this study was to investigate how NAg can contribute to neuronal cell death. In the study primary cultures of rat cerebellar granule cells (CGC) were used. We tested hypothesis concerning the role of glutamatergic NMDA receptors in NAg-evoked neurotoxicity. In our study changes in intracellular calcium (Ca2+) homeostasis, uptake of 45Ca2+, reactive oxygen species (ROS) production, mitochondrial membrane potential and cells viability were investigated. We used commercially available 0.2% polyvinylpyrrolidone (PVP)-coated NAg <100 nm. To avoid sedimentation and agglomeration, before application to the CGC culture, NAg were sonicated with fetal calf serum. NAg were applied in concentration 2.5–75 µg/ml for 10, 30 min or 24 h, depending on experiment. As a pharmacological tool 0.5 µM MK801, a noncompetitive inhibitor of NMDA receptor, was used. After 10 min incubation in the presence of 25–75 µg/ ml NAg dose dependent increase of 45Ca2+ concentration was observed in neurons. This increase was comparable to that evoked by 100 µM glutamate and was completely abolished by MK801. Using fluorescent intracellular calcium indicator fluo3 we observed increase in intracellular calcium level by 200% compared to control, which was partially diminished by MK801. ROS production was measured using fluorescent dye DCF. After 30 min incubation with 75 µg/ml NAg the increase by about 35% over control level was observed and application of MK801 reduced it significantly. Changes in mitochondrial membrane potential were determined using rhodamine (R123). We observed significant decrease in mitochondrial potential during 30 min incubation with different concentrations of NAg and also in this case administration of MK801 was protective. Cells viability was assessed after 24 h incubation with NAg µg/ml alone or together with MK801. Application of MK801 increased neuronal survival from 50% up to 80%. Our results show that excitotoxicity via activation of NMDA receptor, followed by calcium imbalance, destabilization of mitochondrial function and ROS production, seems to be important mechanism involved in neurotoxicity evoked by NAg in cultured neurons. Supported by grant NN401619938.

Ograniczanie wyników

Protective effects of nicotine against glutamate-induced neurotoxicity in PC12 cells

The third neurotoxicity caused by organophosphorous pesticides

Rat sciatic nerve lysosomal enzyme activity as a test for noncholinergic neurotoxic effect of Bromphenvinphos

Effects of repeated systemic penicillin injections on nonconvulsive and convulsive epileptic seizures in the rat

The evaluation of the role of mGluR7 in neuronal apoptotic processes by usage of AMN082, a selective mGluR7 agonist and mGluR7 knockout-derived cells

Repeated isoflurane exposures of neonatal rats contribute to cognitive dysfunction in juvenile animals: the role of miR-497 in isoflurane-induced neurotoxicity

Non-Abeta component of Alzheimer's disease amyloid and amyloid beta peptides evoked poly(ADP-ribose) polymerase-dependent release of apoptosis-inducing factor from rat brain mitochondria

Effects of p53 inhibitor on survival and death of cells subjected to oxidative stress

Assessment of neurotoxicity of pharmacological compounds during early neural development of human embryonic stem cells

Essentiality and toxicity of vanadium supplements in health and pathology

Acute cytotoxicity evoked by tetrabromobisphenol A in primary cultures of rat cerebellar granule cells outweighs the effects of polychlorinated biphenyls

Causes of L-cysteine neurotoxicity

The role of nitric oxide in paraquat-induced oxidative stress in rat striatum

How does trimethyltin affect the brain: facts and hypotheses

Effects of 17-beta estradiol and estriol on NMDA-induced toxicity and apoptosis in primary cultures of rat cortical neurons

Calcium transients in brain ischemia : role in neuronal injury

The influence of repeated systemic penicillin injections at subconvulsive doses on spontaneous Spike-Wave Discharges in the rat

The effects of organic solvents on poly[ADP-ribose] polymerase-1 activity: implications for neurotoxicity