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Effect of thimerosal on Ca2+ movement and viability in human oral cancer cellsDepartment of Pathology and Laboratory Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Department of Psychiatry, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, Laboratory Medicine Division, Zuoying Armed Forces General Hospital, Kaohsiung, Taiwan
Department of Nursing, Tzu Hui Institute of Technology; Pingtung, Taiwan
Department of Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Otolaryngology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Pediatrics, Ping Tung Christian Hospital, Ping Tung, Taiwan
Department of Otolaryngology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Otolaryngology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Surgery, Ping Tung Christian Hospital, Ping Tung, Taiwan
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Dentist, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, crjan{at}isca.vghks.gov.tw The effect of thimerosal on cytosolic free Ca2+ concentrations ([Ca2+]i ) in human oral cancer cells (OC2) is unclear. This study explored whether thimerosal changed basal [Ca2+]i levels in suspended OC2 cells using fura-2. Thimerosal at concentrations between 1and 50 µM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca 2+. Thimerosal-induced Ca2+ influx was not blocked by L-type Ca2+ entry inhibitors and protein kinase C modulators (phorbol 12-myristate 13-acetate [PMA] and GF109203X). In Ca2+-free medium, 50 µM thimerosal failed to induce a [Ca2+]i rise after pretreatment with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Inhibition of phospholipase C with U73122 did not change thimerosal-induced [Ca2+]i rises. At concentrations between 5 and 10 µM, thimerosal killed cells in a concentration-dependent manner. The cytotoxic effect of 8 µM thimerosal was potentiated by prechelating cytosolic Ca2+ with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate/acetomethyl (BAPTA/ AM). Flow cytometry data suggested that 1—7 µM thimerosal-induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, thimerosal-induced [Ca2+]i rises by causing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx through non—L-type Ca2+ channels. Thimerosal killed cells in a concentration-dependent manner through apoptosis.
Key Words: apoptosis • Ca2+ • OC2 • oral cells • thimerosal
This version was published on May
1, 2009 Human & Experimental Toxicology, Vol. 28, No. 5,
301-308 (2009) |
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