PMID- 19574005
OWN - NLM
STAT- MEDLINE
DCOM- 20100319
LR  - 20181201
IS  - 1879-1476 (Electronic)
IS  - 0385-8146 (Linking)
VI  - 37
IP  - 1
DP  - 2010 Feb
TI  - Arsenic trioxide-induced apoptosis of Hep-2 cell line through modulating 
      intracellular glutathione (GSH) level.
PG  - 89-94
LID - 10.1016/j.anl.2009.04.016 [doi]
AB  - BACKGROUND: Since 1970s, a Chinese study group at Harbin Medical University First 
      Hospital discovered the anticancer effect of arsenic trioxide (As2O3), it has 
      become evident that apoptotic effects of As2O3 are not restricted to APL cells 
      but also can be observed in other malignant cells in vitro, including non-APL 
      acute myeloid leukemia cells, myeloma cells, and chronic myeloid leukemia cells, 
      as well as various solid-tumor cells, such as esophageal, prostate, and ovarian 
      carcinomas and neuroblastoma cells. OBJECTIVE: To investigated if As2O3 could 
      induce cell death and apoptosis of Hep-2 cells, a laryngeal squamous cell 
      carcinoma (LSCC) cell line. METHODS: Trypan blue exclusion assay, LDH release 
      assay and cytometric method were used for the measurements of cell death and 
      apoptosis. We measured intracellular GSH, ROS and mitochondrial membrane 
      potential to explore the mechanisms of cell death and apoptosis induced by As2O3 
      in Hep-2 cells. RESULTS: Trypan-blue-positive cells and the release of LDH into 
      medium induced by As2O3 increased in a dose- and time-dependent manner. The rates 
      of apoptosis increased induced by As2O3 in a dose- and time-dependent manner. In 
      order to elucidate the mechanisms of cell death and apoptosis induced by As2O3 in 
      Hep-2 cells through GSH, we found that As2O3 induced the decrease of 
      intracellular GSH, increase of ROS and loss of mitochondrial membrane potential. 
      And pretreatment of BSO, an inhibitor of GSH biosynthesis, depleted partly 
      intracellular GSH and increased trypan-blue-positive cells, the release of LDH, 
      apoptosis, ROS and loss of mitochondrial membrane potential. However, 
      pretreatment of GSH had resistance to the changes to some extent as described 
      above. CONCLUSION: As2O3-induced apoptosis of Hep-2 cell line through modulating 
      intracellular GSH level.
CI  - Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
FAU - Cheng, Baohua
AU  - Cheng B
AD  - Jining Medical College, Jining City, Shandong Province, China. 
      apple9red@yahoo.com.cn
FAU - Yang, Xinxin
AU  - Yang X
FAU - An, Liangxiang
AU  - An L
FAU - Gao, Bo
AU  - Gao B
FAU - Liu, Xia
AU  - Liu X
LA  - eng
PT  - Journal Article
DEP - 20090702
PL  - Netherlands
TA  - Auris Nasus Larynx
JT  - Auris, nasus, larynx
JID - 7708170
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Arsenicals)
RN  - 0 (Oxides)
RN  - 0 (Reactive Oxygen Species)
RN  - GAN16C9B8O (Glutathione)
RN  - S7V92P67HO (Arsenic Trioxide)
SB  - IM
MH  - Antineoplastic Agents/administration & dosage/*pharmacology/*therapeutic use
MH  - Apoptosis/*drug effects
MH  - Arsenic Trioxide
MH  - Arsenicals/administration & dosage/*pharmacology/*therapeutic use
MH  - Carcinoma, Squamous Cell/*drug therapy/*pathology
MH  - Cell Line, Tumor
MH  - Glutathione/*metabolism
MH  - Humans
MH  - Intracellular Space/*drug effects/*metabolism
MH  - Laryngeal Neoplasms/*drug therapy/*pathology
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Oxides/administration & dosage/*pharmacology/*therapeutic use
MH  - Reactive Oxygen Species
EDAT- 2009/07/04 09:00
MHDA- 2010/03/20 06:00
CRDT- 2009/07/04 09:00
PHST- 2008/11/29 00:00 [received]
PHST- 2009/02/22 00:00 [revised]
PHST- 2009/04/21 00:00 [accepted]
PHST- 2009/07/04 09:00 [entrez]
PHST- 2009/07/04 09:00 [pubmed]
PHST- 2010/03/20 06:00 [medline]
AID - S0385-8146(09)00126-6 [pii]
AID - 10.1016/j.anl.2009.04.016 [doi]
PST - ppublish
SO  - Auris Nasus Larynx. 2010 Feb;37(1):89-94. doi: 10.1016/j.anl.2009.04.016. Epub 
      2009 Jul 2.