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W jaki sposób występujące w środowisku substancje hormonalnie czynne wpływają na mózg?

100%

Kajta M.

Wszechświat

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2012

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tom 113

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nr 01-03

2

Oestrogen effects on kainate-induced toxicity in primary cultures of rat cortical neurons

63%

Kajta M., Lason W.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 3

3

Antiapoptotic effects of memantine on staurosporine-induced cell damage in neocortical cultured neurons

51%

Jantas-Skotniczna D., Kajta M., Lason W.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

4

Interaction of aryl hydrocarbon receptor-mediated apoptosis of neuronal cells with estrogen receptor signaling

51%

Kajta M., Wojtowicz A. K., Mackowiak M., Lason W.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Aryl hydrocarbon receptor (AhR) may be responsible for dioxin intoxication, which creates severe clinical problems, such as behavioural and cognitive impairments and an increased number of newborns with deformed brains. Thus, activation of AhRs induces neuronal damage, but the mechanism by which this occurs is largely unknown. Because beta-naphthofl avone is an AhR agonist, we evaluated its impact on apoptotic processes in the mouse primary neuronal cell cultures. In order to verify whether AhR-mediated activation of caspase-3 and lactate dehydrogenase (LDH) release were tissue- and age-dependent, we related them to neocortical and hippocampal tissues, both on 1 and 7 days in vitro. In addition to the effects of estrogen receptor (ER) antagonists and selective estrogen receptor modulators (SERMs), the interaction between AhR-induced apoptosis and ER signaling was evaluated by determining the levels and cellular distribution of AhR and ERbeta. beta-naphtofl avone (0.1ñ100 mM) enhanced caspase-3 activity and LDH release in neocortical and hippocampal cells. A high-affi nity ER antagonist, ICI 182,780, and SERM, tamoxifen, enhanced beta-naphtofl avone-mediated apoptosis. Another SERM, raloxifene, and an ERalpha antagonist, methylpiperidino-pyrazole, did not affect beta-naphtofl avone-induced caspase-3 activity. However, they inhibited beta-naphtofl avoneinduced LDH release at late hour post-treatment, thus suggesting delayed control of AhR-mediated neuronal cell death. The apoptotic effects of beta-naphtofl avone were accompanied by increased levels of AhRs, and these receptors colocalized with ERbeta as demonstrated by confocal microscopy. These data provide evidence for direct interaction of the AhR-mediated apoptotic pathway with estrogen receptor signaling, which gives insight into new strategies to treat or prevent AhR-mediated neurotoxicity. This work was supported by the Polish Ministry of Education and Science, grant No. 2P05A 123 30, and also by the Institute of Pharmacology of Polish Academy of Sciences statutory funds.

5

Estrogen interaction with apoptotic effects of tetra-chlorodibenzo-p-dioxin in primary neuronal cell cultures

51%

Kajta M., Jantas-Skotniczna D., Lason W.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

6

The neuroprotective effect of MTEP, a potent and highly selective mGluRS antagonist, on excitotoxic neuronal death

51%

Domin H., Kajta M., Palucha A., Smialowska M.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

7

Impact of raloxifene and 3,3’-diindolylmethane on neuronal cells exposed to hypoxia

51%

Rzemieniec J., Litwa E., Lason W., Kajta M.

Acta Neurobiologiae Experimentalis

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2013

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tom 73

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nr 1

During the neonatal period of life, hypoxia appears as a major risk factor which may result in complex cerebral dysfunctions like cerebral palsy or seizure disabilities. Natural neuroprotection against hypoxia-induced injury in females is considered to be due to the effects of circulating ovarian hormones, which are lost after ovariectomy or reproductive senescence. Although anti-hypoxic effects of estrogen have been documented, its clinical use has certain limitations. Selective estrogen receptor modulators (SERMs) and selective aryl hydrocarbon receptor modulators (SAhRs) may act as receptor agonists or antagonists in a tissue-specific manner, thus representing a novel approach for the treatment or the prevention of various types of neural degeneration and seizures. In this study we evaluated the mechanism of action of raloxifene and 3,3’-diindolylmethane (DIM) in response to hypoxia in mouse embryonic neuronal cells in primary cultures. Raloxifene is known to bind to estrogen receptors with SERM properties, whereas (DIM) exhibits properties of SAhRs. In our study, hypoxic conditions (5% CO2/95% nitrogen) induced caspase-3 activity and lactate dehydrogenase (LDH) release in the hippocampal cell cultures. Raloxifene and DIM inhibited the hypoxia-induced LDH release by 10–51% and 9–61%, respectively. DIM inhibited also the hypoxia-induced caspase-3 activity by 2–18%, but raloxifene did not affect the hypoxia-induced apoptotic parameter. In our model of hypoxia, estrogen receptor alpha (ER alpha) antagonist MPP (0.01 µM) did not reverse raloxifene-mediated neuroprotection. However, a high-affinity estrogen receptor beta (ER beta) antagonist, PHTPP (0.01 μM), and G-protein coupled receptor 30 antagonist (GPR30), G-15 (0.01 µM), enhanced the neuroprotective effects of raloxifene, which point to neurotoxic potential of ER beta and GPR30 activation in hypoxia. Selective antagonist of aryl hydrocarbon receptors (AhR) alpha-naphthoflavone (1 µM) did not influence neuroprotective action of DIM, thus suggesting AhR-independent effect. These data demonstrated strong neuroprotective potential of raloxifene and DIM which may represent novel therapeutic tools for brain exposed to hypoxic insults. This study was supported by the Polish National Center of Science grant No 2011/01/N/NZ3/04786

8

Effects of estrone on quisqualate-induced toxicity in primary cultures of rat cortical neurons

51%

Kajta M., Marszal M., Kubera M., Lason W.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 2

Estrogens exert protective effects against neurotoxic changes induced by over-activation of ionotrophic glutamate receptors, whereas little is known about their interaction with changes mediated by metabotropic glutamate receptors. We evaluated effects of estrone on quisqualate (QA)-induced toxicity in neuronal cell cultures on 7 and 12 day in vitro (DIV). Twenty four hour exposure to QA (150 µM and 300 µM) significantly decreased cell survival in 7 day old cultures, but the 12 day old cultures were more resistant to its toxicity. DNQX (10 µM), an AMPA/kainate receptor antagonist, partly attenuated the toxic effects of QA, whereas LY 367 385 (100 µM), a selective mGluR1alpha antagonist, completely reversed the above effect. QA did not activate, but suppressed spontaneous caspase-3-like activity. Estrone (100 nM and 500 nM) attenuated QA-mediated neurotoxic effects independently of estrogen receptors, as indicated with ICI 182, 780 and without affecting the caspase-3-like activity. At early stage of development in vitro (7 DIV) toxic effects of QA were more profound and mediated mainly by metabotropic glutamate receptors of group I, whereas later (12 DIV) they were mediated mostly by ionotropic AMPA/kainate receptors. The toxic effects of QA were partly accompanied by anti-apoptotic action against spontaneous caspase-3-like activity, possibly due to modulation of neuronal plasticity.

9

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

51%

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

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 3

10

DDT- and DDE-induced disruption of ovarian steroidogenesis in prepubertal porcine ovarian follicles: a possible interaction with the main steroidogenic enzymes and estrogen receptor ß

51%

Wojtowicz A. K., Kajta M., Gregoraszczuk E. L.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

We evaluated impact of DDT isomers, o, p'- DDT [1, 1-dichloro-2, 2-bis (p, p'-chlorophenyl) ethylene] and p, p'-DDT [1, 1, 1-trichloro-2, 2-bis (p-chlorophenyl) ethane], and their metabolites, o, p'-DDE and p, p'-DDE, on ovarian steroidogenesis. All these compounds, except for p, p'-DDT, demonstrated estrogenic effects on steroid secretion in co-cultures of porcine prepubertal granulosa and theca cells. p,p'-DDT decreased progesterone and estradiol release, which was reversed by the addition of testosterone. In contrast, o, p'-DDT inhibited progesterone secretion with parallel stimulation of basal and testosterone-stimulated estradiol release. DDEs stimulated progesterone and estradiol secretion. The fluorometric assay confirmed that p,p'-DDE, o,p'-DDT, and o,p'-DDE stimulated aromatase activity. Western blots indicated that o,p-DDT and o,p'-DDE diminished the expression of estrogen receptor ß (ERß). This study demonstrated the isomer-dependent action of DDT in pig ovarian cells. We propose that DDT could disrupt ovarian steroidogenesis either by interfering with main steroidogenic enzymes or affecting ERß.

11

A role of nitric oxide in preovulatory decline of oestradiol release by in vitro cultured rat ovarian follicles

51%

Kajta M., Stoklosowa S., Lason W.

Folia Histochemica et Cytobiologica. Supplement

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1997

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tom 35

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nr 2

12

Pretreatment is not mandatory for neuroprotection with 1alpha,25-dihydroxyvitamin D3 in perinatal hypoxic-ischemic rat brain damage in vivo and in excitotoxic injury of primary neuronal cell cultures

33%

Makarewicz D., Kajta M., Zieminska E., Jantas D., Domin H., Lason W., Kutner A., Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

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2009

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tom 69

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nr 1

Previous in vivo and in vitro studies demonstrated neuroprotective potential of pretreatment with 1α, 25-dihydroxyvitamin D3 (calcitriol). The aim of present study was to determine effectiveness of calcitriol administered in vivo after brain ischemic episode in the rat model of perinatal asphyxia, or co-applied with some delay during 24 h exposure to glutamate of the mice hippocampal, cortical and cerebellar neuronal cultures at 7th and 12th day in vitro. In some experiments calcitriol was given after acute exposure to glutamate of the rat cerebellar neurons. Our results demonstrated, that in the 7 day old rat pups submitted to hypoxia ñ ischemia acute application of calcitriol in one dose of 2 μg/kg 30 min after termination of the insult or sub-chronic, 7-day post-treatment with calcitriol effectively diminished brain damage. The rate of such accomplished neuroprotection exceeded that achieved by hypoxic preconditioning, used as the reference neuroprotective method. Moreover the results of our in vitro experiments revealed the ability of calcitriol to reduce excitotoxicity in a way dependent on origin of neuronal cells, stage of their development and duration of excitotoxic insult. Calcitriol was neuroprotective when it was applied together with glutamate or even with up to 6 h delay during 24-h excitotoxic challenge to the hippocampal and neocortical, but not cerebellar neuronal cultures. In addition calcitriol inhibited glutamate-induced caspase-3 activity in hippocampal cultures. We ascribe these protective effects of calcitriol to a rapid, possibly non-genomic modulation by this compound of the mechanisms that are instrumental in its direct neuroprotective action. The study was supported by Polish MNSW Scientifi c Network Fund no 26/E-40/SN-0023/2007

Ograniczanie wyników

W jaki sposób występujące w środowisku substancje hormonalnie czynne wpływają na mózg?

Oestrogen effects on kainate-induced toxicity in primary cultures of rat cortical neurons

Antiapoptotic effects of memantine on staurosporine-induced cell damage in neocortical cultured neurons

Interaction of aryl hydrocarbon receptor-mediated apoptosis of neuronal cells with estrogen receptor signaling

Estrogen interaction with apoptotic effects of tetra-chlorodibenzo-p-dioxin in primary neuronal cell cultures

The neuroprotective effect of MTEP, a potent and highly selective mGluRS antagonist, on excitotoxic neuronal death

Impact of raloxifene and 3,3’-diindolylmethane on neuronal cells exposed to hypoxia

Effects of estrone on quisqualate-induced toxicity in primary cultures of rat cortical neurons

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

DDT- and DDE-induced disruption of ovarian steroidogenesis in prepubertal porcine ovarian follicles: a possible interaction with the main steroidogenic enzymes and estrogen receptor ß

A role of nitric oxide in preovulatory decline of oestradiol release by in vitro cultured rat ovarian follicles

Pretreatment is not mandatory for neuroprotection with 1alpha,25-dihydroxyvitamin D3 in perinatal hypoxic-ischemic rat brain damage in vivo and in excitotoxic injury of primary neuronal cell cultures