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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Involvement of intracellular free Ca2+ in enhanced release of herpes simplex virus by hydrogen peroxide | Virology Journal BioMed Central Research Involvement of intracellular free Ca2 in enhanced release of herpes simplex virus by hydrogen peroxide Emiko Arimoto1 Soichi Iwai1 Tetsuro Sumi1 Yuzo Ogawa2 and Yoshiaki Yura 1 Open Access Address Department of Oral and Maxillofacial Surgery II Osaka University Graduate School of Dentistry Osaka Japan and 2Department of Pathology Osaka University Graduate School of Dentistry Osaka Japan Email Emiko Arimoto - arimoto@tenriyorozu-hp.or.jp Soichi Iwai - s-iwai@dent.osaka-u.ac.jp Tetsuro Sumi - sumi@dent.osaka-u.ac.jp Yuzo Ogawa-ogawa@dent.osaka-u.ac.jp Yoshiaki Yura -yura@dent.osaka-u.ac.jp Corresponding author Published 31 August 2006 Received 05 June 2006 Accepted 31 August 2006 Virologyjournal 2006 3 62 doi l0.l I86 I743-422X-3-62 This article is available from http www.virologyj.cOm content 3 1 62 2006 Arimoto et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background It was reported that elevation of the intracellular concentration of free Ca2 Ca2 i by a calcium ionophore increased the release of herpes simplex virus type 1 HSV-1 . Freely diffusible hydrogen peroxide H2O2 is implied to alter Ca2 homeostasis which further enhances abnormal cellular activity causing changes in signal transduction and cellular dysfunction. Whether H2O2 could affect Ca2 i in HSV-1-infected cells had not been investigated. Results H2O2 treatment increased the amount of cell-free virus and decreased the proportion of viable cells. After the treatment an elevation in Ca2 i was observed and the increase in Ca2 i was suppressed when intracellular and cytosolic Ca2 were buffered by Ca2 chelators. In the presence of Ca2 chelators H2O2-mediated increases of cell-free virus and cell death were .
