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Bisphenol A에 의한 신경계 세포의 칼슘 항상성 교란 및 세포독성에 미치는 영향
이윷모(Yoot Mo Lee),이상민(Sang Min Lee),손동주(Dong Ju Son),이선영(Sun Young Lee),박혜지(Hye Ji Park),남상윤(Sang Yun Nam),김대중(Dae Joong Kim),윤영원(Young Won Yun),유환수(Hwan Soo Yoo),오기완(Ki Wan Oh),김태성(Tae Seong Kim),한순영( 한국독성학회 2004 Toxicological Research Vol.20 No.3
We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration.<br/> Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of<br/> environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic<br/> agents which cause increase of intracellular calcium level, BPA decreased [Ca2+]i dose-dependently<br/> in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at<br/> greater concentrations than 100 μM reduced cell viability significantly in both types of cells. BPA also<br/> suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist,<br/> 30 μM)-induced increase of [Ca2+]i. BPA further lowered caffeine (RYR activator, 100 μM)-decreased<br/> [Ca2+]i, but did not alter dantrolene (RYR inhibitor, 100 μM), heparin (IP3 inhibitor, 200 units/ml) and<br/> xestospongin C (IP3 inhibitor, 5 μM)-decreased [Ca2+]i. Cell viability was not directly related to intracellular<br/> calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal<br/> factor of BPA-induced neuronal cell death.
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Glutamate에 의한 세포내 칼슘농도변화와 세포독성과의 관계
황인영,신임철,송연숙,성민제,박혜지,이윷모,박철범,이명구,오기완,심영용,홍진태 한국독성학회 2002 Toxicological Research Vol.18 No.4
Pathophysiological elevation of intracellular calcium concentration ([Ca^(2+)]_i) in the neuron has been considered as an important responsible factor in the neuronal cell damages. However, the mechanism of increase of [Ca^(2+)]_i and the relationship between [Ca^(2+)]_i level and cytotocixity have not been fully demonstrated. In the present study, real-time alteration of [Ca^(2+)]_i and cellular response (cell damages) in the pheochromocytoma cells (PC12) stimulated by glutamate were investigated. Glutamate dose dependently decreased cell viability determined propidium iodide fluorescence method and morphology change. Choversely related with cell damages, glutamate dose dependently increased the level of [Ca^(2+)]_i. To investigate the mechanism of glutamate-induced increase of [Ca^(2+)]_i, [Ca^(2+)]_i was first measured in the cells cultured in calcium free media and in the presence of dantrolene, an inhibitor of calcium release from ryanodine receptor located in endoplasmic reticulum (ER). Similar to the increase [Ca^(2+)]_i in the calcium-containing media, glutamate does dependently increased [Ca^(2+)]_i in the cells cultured in free calcium media. However, pretreatment (2hr) with 20~50μM dantrolene substantial lowered glutamate-induced increase of [Ca^(2+)]_i, suggesting that release of calcium from ER may be major sourse of increase of [Ca^(2+)]_i in PC12 cells. Dantrolene-induced inhibition of [Ca^(2+)]_i resulted in recovery of cytotoxicity by glutamate. Relevance of N-methyl-D-aspartate (NMDA) receptor, a type of glutamate receptor on glutamate-induced increase of [Ca^(2+)]_i, [Ca^(2+)]_i was also determined in the cells pretreated (2hr) with NMDA receptor antagonist MK-801. Glutamate-induced increase of [Ca^(2+)]_i was reduced by MK-801 dose dependently. Furthermore, glutamate-induced cytotoxicity was also provented by MK-801. These results demonstrate that glutamate increase [Ca^(2+)]_i dose dependently and thereby cause cytotoxicity. The increase of [Ca^(2+)]_i may release from ER, especially through ryanodine receptor and/or through NMDA receptor. Alteration of calcium homeostasis through disturbance of ER system and/or calaium influx through NMDA receptor could contribute glutamate-induced cell damages.
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미성숙 마우스에 Bisphenol A 노출시 신경내분비계에서 에스트로겐 수용체 발현 및 신경행동 변화
성민제(Min Jae Seoung),신임철(Im Cheol Shin),이윷모(Yoot Mo Lee),손동주(Dong Ju Son),송연숙(Youn Sook Song),전계현(Kei Hyun Jeon),김윤배(Yun Bae Kim),이법준(Beum Jun Lee),김대중(Dae Joong Kim),윤영원(Young Won Yun),김태성(Tae Seong K 한국독성학회 2004 Toxicological Research Vol.20 No.3
A large number of chemical pollutants including phthalates, alkylphenolic compounds<br/> and organochlorine pesticides have the ability to disrupt endocrine function in animals, and alter cognitive<br/> function. Because hormone mediated events play an important role in central nervous system<br/> development and function, the changes in cognitive function seem to be mediated by the endocrinelike<br/> action of these chemicals. The present study therefore was designed to investigate effect of<br/> bisphenol A (BPA), an endocrine disrupting chemical on neuro-behavial patterns, and expression of<br/> estrogen receptors and tyrosine hydroxylase, a limiting enzyme of dopamine synthesis pathway. BPA<br/> was treated orally for 3 weeks into 3 week old mice, and then the neuro-behavial patterns (stereotype<br/> behaviors such as jumping rearing and forepaw tremor, climbing behavior, tail flick, rotarod and<br/> locomotor activity), and the expression of estrogen receptors and tyrosine hydroxylase were determined<br/> every 3 week for 9 weeks. During the treatment of BPA, the food uptake and body weight<br/> increase were not significantly changed. BPA resulted in the increased stereotype behaviors (jumping,<br/> rearing and forepaw tremor) 6 or 9 weeks after treatment. The time response to tail flick and<br/> locomotor activity were decreased by the treatment of BPA, whereas the time for rotarod was<br/> increased by the treatment of BPA. The expression of estrogen receptor alpha and beta was<br/> increased in the brain and pituitary gland. Maximum expression was found in the brain after 9 week<br/> of 100 mg/kg BPA treatment and in the pituitary gland after 6 week of 100 mg/kg BPA treatment.<br/> Tyrosine hydroxylase was increased in dose and time dependent manners in the brain but no change<br/> was found in the pituitary gland. The present data show that exposure of BPA in the young mice<br/> could alter expression of estrogen receptors and dopamine synthesis pathway, thereby modulate<br/> neuro-behavial patterns (increase of stereotype behaviors but decrease locomotor activity).
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