KMID : 0379520040200030241
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Çѱ¹µ¶¼ºÇÐȸÁö 2004 Volume.20 No. 3 p.241 ~ p.250
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Bisphenol A Disturbs Intracellular Calcium Homeostasis and its Relationship with Cytotoxicity
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Lee Yuk-Mo
Lee Sang-Min Son Dong-Joo Lee Sun-Young Park Hye-Ji Nam Sang-Yoon Kim Dae-Joong Yun Young-Won Yoo Hwan-Soo Oh Ki-Wan Kim Tae-Sung Han Soon-Young Hong Jin-Tae
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Abstract
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We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration. Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic agents which cause increase of intracellular calcium level, BPA decreased [Ca^{2+}]_i dose-dependently in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at greater concentrations than 100 mutextrm{M} reduced cell viability significantly in both types of cells. BPA also suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist, 30 mutextrm{M})-induced increase of [Ca^{2+}]_i. BPA further lowered caffeine (RYR activator, 100 mutextrm{M})-decreased [Ca^{2+}]_i, but did not alter dantrolene (RYR inhibitor, 100 mutextrm{M}), heparin (IP3 inhibitor, 200 units/ml) and xestospongin C (IP3 inhibitor, 5 mutextrm{M})-decreased [Ca^{2+}]_i. Cell viability was not directly related to intracellular calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal factor of BPA-induced neuronal cell death.
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KEYWORD
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Sisphenol A, Calcium homeostasis, Neurotoxic mechanism
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