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1

Neurotoxic effect of copper salts in rats

100%
Plech A., Klimkiewicz T., Jakrzewska H.
Polish Journal of Environmental Studies
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2000
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tom 09
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nr 4
Neurotoxic effects of copper ions after intraperitoneal (ip) and intracerebroventricular (icv) injections of CuSO4 • 5H2O and Cu(CH,COO) 2 • H2O at doses of 1-100 nmols icv and 0.1-100 pmols/kg ip was deter­mined in rats using two behavioural methods: exploratory and locomotor activity in an open field test and spatial memory in a water maze test. It has been found that higher doses of copper salts (100 nmols icv and 100 ^mols/kg ip) significantly decreased spatial memory of rats.
2
Content available remote

3-Fluoromethcathinone, a structural analog of mephedrone, inhibits growth and induces cell cycle arrest in HT22 mouse hippocampal cells

86%
Siedlecka-Kroplewska K., Szczerba A., Lipinska A., Slebioda T., Kmiec Z.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 2
3
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Competitive and non-competitive NMDA receptor antagonists induce c-Fos expression in the rat anterior, cingulate cortex

86%
Wedzony K., Czyrak A.
Journal of Physiology and Pharmacology
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1996
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tom 47
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nr 3
4
Content available remote

Intermingled modulatory and neurotoxic effects of thimerosal and mercuric ions on electrophysiological responses to GABA and NMDA in hippocampal neurons

72%
Wyrembek P., Szczuraszek K., Majewska M. D., Mozrzymas J. W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 6
5
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Neurotoxic effect of dermally applied chlorpyrifos and cypermethrin. Reversibility of changes

72%
Latuszynska J., Luty S., Raszewski G., Przebirowska D., Tokarska-Rodak M.
Annals of Agricultural and Environmental Medicine
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2003
|
tom 10
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nr 2
6
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Neurotoxic effect of dermally-applied chlorpyrifos and cypermethrin in Wistar rats

72%
Latuszynska J., Luty S., Raszewski G., Tokarska-Rodak M., Przebirowska D., Przylepa E., Haratym-Maj A.
Annals of Agricultural and Environmental Medicine
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2001
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tom 08
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nr 2
7

Degradation of ochratoxin A by Lactobacillus acidophilus K1

58%
Mazurkiewicz J.
Electronic Journal of Polish Agricultural Universities. Series: Biotechnology
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2011
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tom 14
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nr 2
8

Activation of the heat shock response in a primary cellular model of motoneuron neurodegeneration - evidence for neuroprotective and neurotoxic effects

58%
Kalmar B., Greensmith L.
Cellular and Molecular Biology Letters
|
2009
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tom 14
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nr 2
Pharmacological up-regulation of heat shock proteins (hsps) rescues motoneurons from cell death in a mouse model of amyotrophic lateral sclerosis. However, the relationship between increased hsp expression and neuronal survival is not straightforward. Here we examined the effects of two pharmacological agents that induce the heat shock response via activation of HSF-1, on stressed primary motoneurons in culture. Although both arimoclomol and celastrol induced the expression of Hsp70, their effects on primary motoneurons in culture were significantly different. Whereas arimoclomol had survival-promoting effects, rescuing motoneurons from staurosporin and H2O2 induced apoptosis, celastrol not only failed to protect stressed motoneurons from apoptosis under same experimental conditions, but was neurotoxic and induced neuronal death. Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. These results indicate that not all agents that activate the heat shock response will necessarily be neuroprotective.
9

Acute lead toxicity and energy metabolism in rat brain synaptosomes

58%
Struzynska L., Dabrowska-Bouta B., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 4
10

Effect of combined prenatal exposure to aluminium and ethanol on central dopamine, serotonin and muscarine receptor reactivity in rats

58%
Brus R., Szkilnik R., Nowak P., Mikolajun U., Tramer W., Mengel K.
Polish Journal of Environmental Studies
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1997
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tom 06
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nr 2
Ethanol (EtOH) abuse in pregnancy is know to seriously damage the internal organs of the fetus, a condition in humans that is classified as "fetal alcohol syndrome". Aluminium (Al) can develop neurotoxic effects and contribute to some neurological disorders. To test whether the reactivity of some central receptors (dopamine - DA, serotonin-5-HT and muscanne - M) may be altered by prenatal EtOH and Al, administered separately or jointly, female rats were given 10% (v/v) EtOH and/or Al(600 or 3000 ppm) throughout pregnancy in their drinking water. Male adult offspring were tested at 3 months for behavioural effects know to be induced by agonists acting at different subtypes of DA (D1 D2, D3,), 5-HT2t and M receptors. Addition antagonist of D, receptor have been examined. The substances SKF 38393, quinpirole, mCPP, pilocarpine, haloperidol, and the behavioral procedures of yawning, oral activity and catalepsy have been used for assessment. The results of the experiment indicate that EtOH does not modify the effect of the central DA and M receptor agonist and DA antagonist in Al prenataly exposed rats. On the other hand, EtOH modified the reactivity of the central 5-HT2c receptor to agonist (mCPP) in Al pretreated rats.
11
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Dermal and oral toxicity of malathion in rats

58%
Tos-Luty S., Obuchowska-Przebirowska D., Latuszynska J., Tokarska-Rodak M., Haratym-Maj A.
Annals of Agricultural and Environmental Medicine
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2003
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tom 10
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nr 1
The aim of the study was the evaluation of dermal and oral toxicity of malathion based on the results of histopathologic and ultrastructural tests. The standard of the pesticide - IPO 460 Malathion was used in the study. The preparation was suspended in oil emulsion. The study was conducted on Wistar rats. Dermal toxicity was examined in 2 groups of experimental rats. The animals were applied 8 mg (1/100 LD50) and 16 mg (1/50 LD50) of the preparation on the tail skin for 4 hours daily for a period of 28 days. In the case of oral toxicity, a dose of 1/50 LD50 malathion was used. The amount of 1 ml (11.2 g) of the preparation was administered intragastrically by stomach tube for 28 days. In both experiments the control animals were administered only the emulsion used for suspending the pesticide. The following organs were subject to histopathologic and ultrastructural evaluation: liver, kidneys, heart and lungs. The histopathologic and ultrastructural changes observed showed various degrees of intensity according to the route of malathion administration and the size of the dose applied. Dermal application of the pesticide in a smaller dose did not cause histopathological changes in the organs of the animals, while the administration of a higher dose resulted in changes only in the liver. Changes on the ultrastructural level occurred in all organs and were dose-dependent. After oral administration of malathion, both histopathologic and ultrastructural changes observed in all organs were more intensified than after dermal application.
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