NDLI: Reactive oxygen species from mitochondria mediate SW480 cells apoptosis induced by Na$_{2}$SeO$

Content Provider	Springer Nature Link
Author	Wang, Hai Tao Yang, Xiang Liang Zhang, Zhi Hong Lu, Jing Ling Xu, Hui Bi
Copyright Year	2002
Abstract	A number of selenium compounds have been found to inhibit tumorigenesis in a variety of animal and cell models. In order to explore the molecular mechanism involved in the anticarcinogenesis activity of selenium, we examined the effects of sodium selenite on cell viabilty, generation of reactive oxygen species (ROS), and mitochondrial transmembrane potential (Δω$_{ m }$) in human colonic carcinoma cells SW480. The result from MTT test showed that sodium selenite reduced cell viability. Morophologic and flow cytometric results indicated that Na$_{2}$SeO$_{3}$ induced the apoptosis of SW480 cells. Na$_{2}$SeO$_{3}$ increased the generation of intracellular ROS, whereas BAPTA-AM, rotenone, and NaCN completely inhibited the increase of ROS induced by Na$_{2}$SeO$_{3}$. Na$_{2}$SeO$_{3}$ also caused the disruption of Δω$_{ m }$. The intracellular ROS increase and apoptosis induced by Na$_{2}$SeO$_{3}$ were significantly decreased by superoxide dismutase (SOD), catalase. These data suggest that the ROS mediate apoptosis induced by Na$_{2}$SeO$_{3}$ and mitochondria may be a major source of Na$_{2}$SeO$_{3}$-induced ROS.
Starting Page	241
Ending Page	254
Page Count	14
File Format	PDF
ISSN	01634984
Journal	Biological Trace Element Research
Volume Number	85
Issue Number	3
e-ISSN	15590720
Language	English
Publisher	Humana Press
Publisher Date	2002-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Biochemistry Biotechnology Nutrition Oncology
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Endocrinology, Diabetes and Metabolism Clinical Biochemistry Biochemistry Inorganic Chemistry

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