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of chlorzoxazone on Ca2+movement and viability in human oral cancer cells.\nChlorzoxazone is a skeletal muscle relaxant. However, the effect of chlorzoxazone on intracellular Ca2+ concentrations ([Ca2+]i) in oral cancer cells is unclear. This study examined whether chlorzoxazone altered Ca2+ signaling and cell viability in OC2 human oral cancer cells. [Ca2+]iin suspended cells was measured using the fluorescent Ca2+-sensitive dye fura-2. Cell viability was examined by water-soluble tetrazolium-1 assay. Chlorzoxazone (250-1000 μM) induced [Ca2+]irises in a concentration-dependent manner. Ca2+ removal reduced the signal by approximately 50%. Mn2+ has been shown to enter cells through similar mechanisms as Ca2+ but quenches fura-2 fluorescence at all excitation wavelengths. Chlorzoxazone (1000 μM) induced Mn2+ influx, suggesting that Ca2+ entry occurred. Chlorzoxazone-induced Ca2+ entry was inhibited by 20% by inhibitors of store-operated Ca2+ channels and protein kinase C (PKC) modulators. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (TG) inhibited chlorzoxazone-evoked [Ca2+]irises by 88%. Conversely, treatment with chlorzoxazone-suppressed TG-evoked [Ca2+]irises 75%. Chlorzoxazone induced [Ca2+]irises by exclusively releasing Ca2+ from the endoplasmic reticulum. Inhibition of phospholipase C (PLC) with U73122 did not alter chlorzoxazone-induced [Ca2+]irises. PLC activity was not involved in chlorzoxazone-evoked [Ca2+]irises. Chlorzoxazone at 200-700 μM decreased cell viability, which was not reversed by pretreatment with Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl. In sum, in OC2 cells, chlorzoxazone induced [Ca2+]irises by evoking PLC-independent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. Chlorzoxazone also caused Ca2+-independent cell death. Since [Ca2+]irises play a triggering or modulatory role in numerous cellular phenomena, the effect of chlorzoxazone on [Ca2+]iand cell viability should be taken into account in other in vitro studies."}

{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":127,"end":243},"obj":"DRI_Approach"},{"id":"T2","span":{"begin":244,"end":359},"obj":"DRI_Background"},{"id":"T3","span":{"begin":448,"end":513},"obj":"DRI_Background"},{"id":"T4","span":{"begin":600,"end":653},"obj":"DRI_Background"},{"id":"T5","span":{"begin":654,"end":787},"obj":"DRI_Background"},{"id":"T6","span":{"begin":870,"end":891},"obj":"REPLACED"},{"id":"T7","span":{"begin":897,"end":940},"obj":"DRI_Background"},{"id":"T8","span":{"begin":961,"end":1008},"obj":"DRI_Background"},{"id":"T9","span":{"begin":1009,"end":1160},"obj":"DRI_Background"},{"id":"T10","span":{"begin":1241,"end":1337},"obj":"DRI_Background"},{"id":"T11","span":{"begin":1338,"end":1435},"obj":"DRI_Approach"},{"id":"T12","span":{"begin":1436,"end":1503},"obj":"DRI_Background"},{"id":"T13","span":{"begin":1504,"end":1601},"obj":"DRI_Approach"},{"id":"T14","span":{"begin":1623,"end":1653},"obj":"DRI_Approach"},{"id":"T15","span":{"begin":1681,"end":1688},"obj":"DRI_Approach"},{"id":"T16","span":{"begin":1689,"end":1756},"obj":"DRI_Approach"},{"id":"T17","span":{"begin":1778,"end":1835},"obj":"DRI_Approach"},{"id":"T18","span":{"begin":1870,"end":1876},"obj":"DRI_Approach"},{"id":"T19","span":{"begin":1877,"end":1931},"obj":"DRI_Background"},{"id":"T20","span":{"begin":1932,"end":2132},"obj":"DRI_Background"}],"text":"Action of chlorzoxazone on Ca2+movement and viability in human oral cancer cells.\nChlorzoxazone is a skeletal muscle relaxant. However, the effect of chlorzoxazone on intracellular Ca2+ concentrations ([Ca2+]i) in oral cancer cells is unclear. This study examined whether chlorzoxazone altered Ca2+ signaling and cell viability in OC2 human oral cancer cells. [Ca2+]iin suspended cells was measured using the fluorescent Ca2+-sensitive dye fura-2. Cell viability was examined by water-soluble tetrazolium-1 assay. Chlorzoxazone (250-1000 μM) induced [Ca2+]irises in a concentration-dependent manner. Ca2+ removal reduced the signal by approximately 50%. Mn2+ has been shown to enter cells through similar mechanisms as Ca2+ but quenches fura-2 fluorescence at all excitation wavelengths. Chlorzoxazone (1000 μM) induced Mn2+ influx, suggesting that Ca2+ entry occurred. Chlorzoxazone-induced Ca2+ entry was inhibited by 20% by inhibitors of store-operated Ca2+ channels and protein kinase C (PKC) modulators. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (TG) inhibited chlorzoxazone-evoked [Ca2+]irises by 88%. Conversely, treatment with chlorzoxazone-suppressed TG-evoked [Ca2+]irises 75%. Chlorzoxazone induced [Ca2+]irises by exclusively releasing Ca2+ from the endoplasmic reticulum. Inhibition of phospholipase C (PLC) with U73122 did not alter chlorzoxazone-induced [Ca2+]irises. PLC activity was not involved in chlorzoxazone-evoked [Ca2+]irises. Chlorzoxazone at 200-700 μM decreased cell viability, which was not reversed by pretreatment with Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl. In sum, in OC2 cells, chlorzoxazone induced [Ca2+]irises by evoking PLC-independent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. Chlorzoxazone also caused Ca2+-independent cell death. Since [Ca2+]irises play a triggering or modulatory role in numerous cellular phenomena, the effect of chlorzoxazone on [Ca2+]iand cell viability should be taken into account in other in vitro studies."}

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sapiens"},{"id":"T51","span":{"begin":1821,"end":1824},"obj":"CVCL_B845|Embryonic_stem_cell|Homo sapiens"},{"id":"T52","span":{"begin":1865,"end":1868},"obj":"CVCL_B845|Embryonic_stem_cell|Homo sapiens"},{"id":"T53","span":{"begin":1903,"end":1906},"obj":"CVCL_B845|Embryonic_stem_cell|Homo sapiens"},{"id":"T54","span":{"begin":1939,"end":1942},"obj":"CVCL_B845|Embryonic_stem_cell|Homo sapiens"},{"id":"T55","span":{"begin":1956,"end":1957},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T56","span":{"begin":2052,"end":2055},"obj":"CVCL_B845|Embryonic_stem_cell|Homo sapiens"}],"text":"Action of chlorzoxazone on Ca2+movement and viability in human oral cancer cells.\nChlorzoxazone is a skeletal muscle relaxant. However, the effect of chlorzoxazone on intracellular Ca2+ concentrations ([Ca2+]i) in oral cancer cells is unclear. This study examined whether chlorzoxazone altered Ca2+ signaling and cell viability in OC2 human oral cancer cells. [Ca2+]iin suspended cells was measured using the fluorescent Ca2+-sensitive dye fura-2. Cell viability was examined by water-soluble tetrazolium-1 assay. Chlorzoxazone (250-1000 μM) induced [Ca2+]irises in a concentration-dependent manner. Ca2+ removal reduced the signal by approximately 50%. Mn2+ has been shown to enter cells through similar mechanisms as Ca2+ but quenches fura-2 fluorescence at all excitation wavelengths. Chlorzoxazone (1000 μM) induced Mn2+ influx, suggesting that Ca2+ entry occurred. Chlorzoxazone-induced Ca2+ entry was inhibited by 20% by inhibitors of store-operated Ca2+ channels and protein kinase C (PKC) modulators. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (TG) inhibited chlorzoxazone-evoked [Ca2+]irises by 88%. Conversely, treatment with chlorzoxazone-suppressed TG-evoked [Ca2+]irises 75%. Chlorzoxazone induced [Ca2+]irises by exclusively releasing Ca2+ from the endoplasmic reticulum. Inhibition of phospholipase C (PLC) with U73122 did not alter chlorzoxazone-induced [Ca2+]irises. PLC activity was not involved in chlorzoxazone-evoked [Ca2+]irises. Chlorzoxazone at 200-700 μM decreased cell viability, which was not reversed by pretreatment with Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl. In sum, in OC2 cells, chlorzoxazone induced [Ca2+]irises by evoking PLC-independent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. Chlorzoxazone also caused Ca2+-independent cell death. Since [Ca2+]irises play a triggering or modulatory role in numerous cellular phenomena, the effect of chlorzoxazone on [Ca2+]iand cell viability should be taken into account in other in vitro studies."}