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  • 1 Kaohsiung Veterans General Hospital Department of Otolaryngology Kaohsiung Taiwan
  • | 2 Chang Gung Institute of Technology Chiayi Campus Institute of Nursing and Department of Nursing Chiayi Taiwan
  • | 3 Tzu Hui Institute of Technology Department of Nursing Pingtung Taiwan
  • | 4 Kaohsiung Veterans General Hospital Department of Dentistry Kaohsiung Taiwan
  • | 5 National Sun Yat-Sen University Department of Biological Sciences Kaohsiung Taiwan
  • | 6 Kaohsiung Veterans General Hospital Department of Medical Education and Research Kaohsiung Taiwan 813
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The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca2+ concentrations ([Ca2+]i) in OC2 human oral cancer cells is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended OC2 cells by using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 10–60 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. M-3M3FBS-induced Ca2+ influx was inhibited by the store-operated Ca2+ channel blockers nifedipine, econazole and SK&F96365, and by the phospholipase A2 inhibitor aristolochic acid. In Ca2+-free medium, 30 μM m-3M3FBS pretreatment inhibited the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin and 2,5-di-tert-butylhydroquinone (BHQ). Conversely, pretreatment with thapsigargin, BHQ or cyclopiazonic acid partly reduced m-3M3FBS-induced [Ca2+]i rise. Inhibition of inositol 1,4,5-trisphosphate formation with U73122 did not alter m-3M3FBS-induced [Ca2+]i rise. At concentrations between 5 and 100 μM m-3M3FBS killed cells in a concentration-dependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA). Propidium iodide staining data suggest that m-3M3FBS (20 or 50 μM) induced apoptosis in a Ca2+-independent manner. Collectively, in OC2 cells, m-3M3FBS induced [Ca2+]i rise by causing inositol 1,4,5-trisphosphate-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-sensitive store-operated Ca2+ channels. M-3M3FBS also induced Ca2+-independent cell death and apoptosis.

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Senior editors

Editor(s)-in-Chief: Rosivall, László

Honorary Editor(s)-in-Chief): Monos, Emil

Managing Editor(s): Bartha, Jenő; Berhidi, Anna

Co-editor(s): Koller, Ákos; Lénárd, László; Szénási, Gábor

Assistant Editor(s): G. Dörnyei (Budapest), Zs. Miklós (Budapest), Gy. Nádasy (Budapest)

Hungarian Editorial Board

    1. Benedek, György (Szeged)
    1. Benyó, Zoltán (Budapest)
    1. Boros, Mihály (Szeged)
    1. Chernoch, László (Debrecen)
    1. Détári, László (Budapest)
    1. Hamar, János (Budapest)
    1. Hantos, Zoltán (Szeged)
    1. Hunyady, László (Budapest)
    1. Imre, Sándor (Debrecen)
    1. Jancsó, Gábor (Szeged)
    1. Karádi, Zoltán (Pécs)
    1. Kovács, László (Debrecen)
    1. Palkovits, Miklós (Budapest)
    1. Papp, Gyula (Szeged)
    1. Pavlik, Gábor (Budapest)
    1. Spät, András (Budapest)
    1. Szabó, Gyula (Szeged)
    1. Szelényi, Zoltán (Pécs)
    1. Szolcsányi, János (Pécs)
    1. Szollár, Lajos (Budapest)
    1. Szücs, Géza (Debrecen)
    1. Telegdy, Gyula (Szeged)
    1. Toldi, József (Szeged)
    1. Tósaki, Árpád (Debrecen)

International Editorial Board

    1. R. Bauer (Jena)
    1. W. Benjelloun (Rabat)
    1. A. W. Cowley Jr. (Milwaukee)
    1. D. Djuric (Belgrade)
    1. C. Fry (London)
    1. S. Greenwald (London)
    1. O. Hänninen (Kuopio)
    1. H. G. Hinghofer-Szalkay (Graz)
    1. Th. Kenner (Graz)
    1. Gy. Kunos (Richmond)
    1. M. Mahmoudian (Tehran)
    1. T. Mano (Seki, Gifu)
    1. G. Navar (New Orleans)
    1. H. Nishino (Nagoya)
    1. O. Petersen (Liverpool)
    1. U. Pohl (Münich)
    1. R. S. Reneman (Maastricht)
    1. A. Romanovsky (Phoenix)
    1. G. M. Rubanyi (Richmond)
    1. T. Sakata (Oita)
    1. A. Siddiqui (Karachi)
    1. Cs. Szabo (Beverly)
    1. E. Vicaut (Paris)
    1. N. Westerhof (Amsterdam)
    1. L. F. Zhang (Xi'an)

Editorial Office:
Akadémiai Kiadó Zrt.
Prielle Kornélia u. 21–35, H-1117 Budapest, Hungary

Editorial Correspondence:
Acta Physiologica Hungarica
Semmelweis University, Faculty of Medicine Institute of Pathophysiology
Nagyvárad tér 4, H-1089 Budapest, Hungary
Phone/Fax: +36-1-2100-100
E-mail: aph@semmelweis-univ.hu

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Acta Physiologica Hungarica
Language English
Size  
Year of
Foundation
1950
Publication
Programme
changed title
Volumes
per Year
 
Issues
per Year
 
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 0231-424X (Print)
ISSN 1588-2683 (Online)

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